Structured Review

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Inhibitors of AKT/eNOS and <t>ERK/VEGF</t> pathways regulate CXCR4 expression and LOC migration. Protein ( a , b ) and mRNA ( c ) expression of CXCR4 measured by Western blotting and real-time PCR on LOCs pretreated with PD98059 (10 μM), GW644652 (10 μM), PX-316 (10 μM), or 7-nitroindazole (10 μM) for 1 h before infection with lenti-miR-126. Representative western blots of CXCR4 ( a ). Quantification of CXCR4 bands on LOCs pretreated with PD98059, GW644652, PX-316, or 7-nitroindazole ( b ). GADPH expression was used for protein level normalization. mRNA expression of CXCR4 ( c ). miR-126 induced LOC migration in response to SDF-1α (100 ng/mL) was dramatically inhibited by PD98059, GW644652, PX-316, or 7-nitroindazole ( d cell count, e crystal violet staining). Data are presented as mean ± SD. *** P
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1) Product Images from "MicroRNA-126 protects against vascular injury by promoting homing and maintaining stemness of late outgrowth endothelial progenitor cells"

Article Title: MicroRNA-126 protects against vascular injury by promoting homing and maintaining stemness of late outgrowth endothelial progenitor cells

Journal: Stem Cell Research & Therapy

doi: 10.1186/s13287-020-1554-9

Inhibitors of AKT/eNOS and ERK/VEGF pathways regulate CXCR4 expression and LOC migration. Protein ( a , b ) and mRNA ( c ) expression of CXCR4 measured by Western blotting and real-time PCR on LOCs pretreated with PD98059 (10 μM), GW644652 (10 μM), PX-316 (10 μM), or 7-nitroindazole (10 μM) for 1 h before infection with lenti-miR-126. Representative western blots of CXCR4 ( a ). Quantification of CXCR4 bands on LOCs pretreated with PD98059, GW644652, PX-316, or 7-nitroindazole ( b ). GADPH expression was used for protein level normalization. mRNA expression of CXCR4 ( c ). miR-126 induced LOC migration in response to SDF-1α (100 ng/mL) was dramatically inhibited by PD98059, GW644652, PX-316, or 7-nitroindazole ( d cell count, e crystal violet staining). Data are presented as mean ± SD. *** P
Figure Legend Snippet: Inhibitors of AKT/eNOS and ERK/VEGF pathways regulate CXCR4 expression and LOC migration. Protein ( a , b ) and mRNA ( c ) expression of CXCR4 measured by Western blotting and real-time PCR on LOCs pretreated with PD98059 (10 μM), GW644652 (10 μM), PX-316 (10 μM), or 7-nitroindazole (10 μM) for 1 h before infection with lenti-miR-126. Representative western blots of CXCR4 ( a ). Quantification of CXCR4 bands on LOCs pretreated with PD98059, GW644652, PX-316, or 7-nitroindazole ( b ). GADPH expression was used for protein level normalization. mRNA expression of CXCR4 ( c ). miR-126 induced LOC migration in response to SDF-1α (100 ng/mL) was dramatically inhibited by PD98059, GW644652, PX-316, or 7-nitroindazole ( d cell count, e crystal violet staining). Data are presented as mean ± SD. *** P

Techniques Used: Expressing, Migration, Western Blot, Real-time Polymerase Chain Reaction, Infection, Cell Counting, Staining

Overexpression of miR-126 activates P13K/Akt/eNOS and ERK/VEGF signaling pathways in LOCs. Western blotting shows immunochemistry signals of ERK, phosphorylated-ERK (p-ERK), VEGF, Akt, p-Akt, and eNOS in LOCs infected with lenti-vector or lenti-miR-126 ( a ). Quantification of p-ERK ( b ), VEGF ( c ), p-Akt ( d ), and eNOS ( e ) bands. GADPH expression was used for protein level normalization for VEGF and eNOS. Data are presented as mean ± SD. * P
Figure Legend Snippet: Overexpression of miR-126 activates P13K/Akt/eNOS and ERK/VEGF signaling pathways in LOCs. Western blotting shows immunochemistry signals of ERK, phosphorylated-ERK (p-ERK), VEGF, Akt, p-Akt, and eNOS in LOCs infected with lenti-vector or lenti-miR-126 ( a ). Quantification of p-ERK ( b ), VEGF ( c ), p-Akt ( d ), and eNOS ( e ) bands. GADPH expression was used for protein level normalization for VEGF and eNOS. Data are presented as mean ± SD. * P

Techniques Used: Over Expression, Western Blot, Infection, Plasmid Preparation, Expressing

Inhibition of miR-126 downregulates protein expression of Akt/eNOS and ERK/VEGF signaling pathways. Western blotting shows immunochemistry signals of phosphorylated-ERK (p-ERK), ERK, VEGF, p-Akt, Akt, and eNOS in LOCs transfected with negative control or miR-126 inhibitor ( a ). Quantification of p-ERK ( b ), VEGF ( c ), p-Akt ( d ), and eNOS ( e ) bands. GADPH expression was used for protein level normalization for VEGF and eNOS. Data are presented as mean ± SD. ** P
Figure Legend Snippet: Inhibition of miR-126 downregulates protein expression of Akt/eNOS and ERK/VEGF signaling pathways. Western blotting shows immunochemistry signals of phosphorylated-ERK (p-ERK), ERK, VEGF, p-Akt, Akt, and eNOS in LOCs transfected with negative control or miR-126 inhibitor ( a ). Quantification of p-ERK ( b ), VEGF ( c ), p-Akt ( d ), and eNOS ( e ) bands. GADPH expression was used for protein level normalization for VEGF and eNOS. Data are presented as mean ± SD. ** P

Techniques Used: Inhibition, Expressing, Western Blot, Transfection, Negative Control

2) Product Images from "Co-expression of HIF-1 and TLR3 is associated with poor prognosis in oral squamous cell carcinoma"

Article Title: Co-expression of HIF-1 and TLR3 is associated with poor prognosis in oral squamous cell carcinoma

Journal: International Journal of Clinical and Experimental Pathology

doi:

IHC analysis of each tumor tissue collected from the OSCC nude mice model. (n=40) OSCC nude mice were treated by inhibition of HIF-1 or NF-κB. A. HIF-1α expression. B. NF-κB expression. C. Ki67 expression. D. VEGF expression (×200).
Figure Legend Snippet: IHC analysis of each tumor tissue collected from the OSCC nude mice model. (n=40) OSCC nude mice were treated by inhibition of HIF-1 or NF-κB. A. HIF-1α expression. B. NF-κB expression. C. Ki67 expression. D. VEGF expression (×200).

Techniques Used: Immunohistochemistry, Mouse Assay, Inhibition, Expressing

3) Product Images from "Dimethyloxaloylglycine Increases the Bone Healing Capacity of Adipose-Derived Stem Cells by Promoting Osteogenic Differentiation and Angiogenic Potential"

Article Title: Dimethyloxaloylglycine Increases the Bone Healing Capacity of Adipose-Derived Stem Cells by Promoting Osteogenic Differentiation and Angiogenic Potential

Journal: Stem Cells and Development

doi: 10.1089/scd.2013.0486

Effect of DMOG on the expression of hypoxia inducible factor-1α ( HIF-1α ) and vascular endothelial growth factor ( VEGF ) in ASCs. (A) Western blotting showed that DMOG significantly affected the protein levels of HIF-1α and VEGF
Figure Legend Snippet: Effect of DMOG on the expression of hypoxia inducible factor-1α ( HIF-1α ) and vascular endothelial growth factor ( VEGF ) in ASCs. (A) Western blotting showed that DMOG significantly affected the protein levels of HIF-1α and VEGF

Techniques Used: Expressing, Western Blot

4) Product Images from "Paired box 5 is a novel marker of breast cancers that is frequently downregulated by methylation"

Article Title: Paired box 5 is a novel marker of breast cancers that is frequently downregulated by methylation

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.27599

PAX5 involved in the regulation of cell cycle pathway and VEGF expression. (A) Western-blot is performed to test the effect of PAX5 on cell cycle pathway and the expression of VEGF. (B) It is shown that PAX5 increases the expression of p53, p21, p27 and decreases the expression of cyclin D1, CDK4, VEGF in breast cancer cells (BT549 and MB231). The values are exhibited as the mean ± SD from three independent experiments (**, p
Figure Legend Snippet: PAX5 involved in the regulation of cell cycle pathway and VEGF expression. (A) Western-blot is performed to test the effect of PAX5 on cell cycle pathway and the expression of VEGF. (B) It is shown that PAX5 increases the expression of p53, p21, p27 and decreases the expression of cyclin D1, CDK4, VEGF in breast cancer cells (BT549 and MB231). The values are exhibited as the mean ± SD from three independent experiments (**, p

Techniques Used: Expressing, Western Blot

5) Product Images from "Therapeutic potential of sustained-release sodium nitrite for critical limb ischemia in the setting of metabolic syndrome"

Article Title: Therapeutic potential of sustained-release sodium nitrite for critical limb ischemia in the setting of metabolic syndrome

Journal: American Journal of Physiology - Heart and Circulatory Physiology

doi: 10.1152/ajpheart.00115.2015

Nitrite therapy promotes angiogenesis during CLI. A and D : message RNA and protein expression of VEGF in control and CLI limb skeletal muscle. B and E : message RNA and protein expression of CD31 (platelet endothelial cell adhesion molecule) in control
Figure Legend Snippet: Nitrite therapy promotes angiogenesis during CLI. A and D : message RNA and protein expression of VEGF in control and CLI limb skeletal muscle. B and E : message RNA and protein expression of CD31 (platelet endothelial cell adhesion molecule) in control

Techniques Used: Expressing

6) Product Images from "Serial Low Doses of Sorafenib Enhance Therapeutic Efficacy of Adoptive T Cell Therapy in a Murine Model by Improving Tumor Microenvironment"

Article Title: Serial Low Doses of Sorafenib Enhance Therapeutic Efficacy of Adoptive T Cell Therapy in a Murine Model by Improving Tumor Microenvironment

Journal: PLoS ONE

doi: 10.1371/journal.pone.0109992

Restoration of immunosuppressive factors in E.G7 cells by sorafenib. (A) (Left panel) Expressions of immunosuppressive factors were assayed by Western blotting, and (right panel) their quantitative results. IDO, VEGF, IL-10 and TGF-βwere decreased in a dose-dependent manner in E.G7 cells treated with 5–15 µM sorafenib for 24 hours. In addition, expressions of pSTAT3 and CCL2/MCP-1 also were decreased. (B) Expression of IDO in E.G7 cells treated with exogenous IFN-γto mimic the tumor-bearing animal model. Sorafenib decreases both endogenous and exogenous IDO expressions. (C) Expression of TGF-βreceptor I was assessed by flow cytometry. TGF-βreceptor I was significant decreased after 2–15 µM sorafenib treatments. (D) Survival of CD8+ T cells would affect the therapeutic outcome of ACT, and apoptosis of CD8+ T cells is mainly through Fas/Fas ligand (FasL) pathway. Thus, expression of FasL was assayed by flow cytometry, and the expression of FasL was suppressed in E.G7 cells by sorafenib. The experiments were repeated more than three times, and one of the representative was shown here. (* as compared with that of vehicle, *p
Figure Legend Snippet: Restoration of immunosuppressive factors in E.G7 cells by sorafenib. (A) (Left panel) Expressions of immunosuppressive factors were assayed by Western blotting, and (right panel) their quantitative results. IDO, VEGF, IL-10 and TGF-βwere decreased in a dose-dependent manner in E.G7 cells treated with 5–15 µM sorafenib for 24 hours. In addition, expressions of pSTAT3 and CCL2/MCP-1 also were decreased. (B) Expression of IDO in E.G7 cells treated with exogenous IFN-γto mimic the tumor-bearing animal model. Sorafenib decreases both endogenous and exogenous IDO expressions. (C) Expression of TGF-βreceptor I was assessed by flow cytometry. TGF-βreceptor I was significant decreased after 2–15 µM sorafenib treatments. (D) Survival of CD8+ T cells would affect the therapeutic outcome of ACT, and apoptosis of CD8+ T cells is mainly through Fas/Fas ligand (FasL) pathway. Thus, expression of FasL was assayed by flow cytometry, and the expression of FasL was suppressed in E.G7 cells by sorafenib. The experiments were repeated more than three times, and one of the representative was shown here. (* as compared with that of vehicle, *p

Techniques Used: Western Blot, Expressing, Animal Model, Flow Cytometry, Cytometry, Activated Clotting Time Assay

Sorafenib augments the therapeutic efficacy of ACT by inhibiting STAT3 expression and downregulating immunosuppressive factors in tumor cells and tumor microenvironment. Downregulation of immunosuppressive factors, including TGF-β, IL-10, CCL2/MCP-1 and VEGF, lowers the populations of both Tregs and MDSCs. Transferred CD8+ T cells show better activation and killing effects due to declined Tregs and MDSCs. Furthermore, more transferred CD8+ T cells accumulate in tumors and survive longer, so that enhanced therapeutic responses can be achieved.
Figure Legend Snippet: Sorafenib augments the therapeutic efficacy of ACT by inhibiting STAT3 expression and downregulating immunosuppressive factors in tumor cells and tumor microenvironment. Downregulation of immunosuppressive factors, including TGF-β, IL-10, CCL2/MCP-1 and VEGF, lowers the populations of both Tregs and MDSCs. Transferred CD8+ T cells show better activation and killing effects due to declined Tregs and MDSCs. Furthermore, more transferred CD8+ T cells accumulate in tumors and survive longer, so that enhanced therapeutic responses can be achieved.

Techniques Used: Activated Clotting Time Assay, Expressing, Activation Assay

WP1066, an STAT3-specific inhibitor, was used to clarify the role of STAT3 in immunosuppressive microenvironment. (A) (Left panel) Expressions of IDO, VEGF, IL-10, and CCL2/MCP-1 were assayed with Western blotting, and (right panel) their quantitative results. All proteins were suppressed after treated with WP1066. (B, C) Expressions of tomato fluorescent protein and intracellular IFN-γwere assayed by flow cytometry. Significantly higher tomato fluorescent protein and IFN-γsignals were found in CD8+ T cells co-cultured with sorafenib and WP1066-treated E.G7 cells, respectively. (D) Effect of WP1066 on migration of CD8+ T cells was evaluated with transwell assay. More migratory CD8+ T cells were found in WP1066-treated E.G7 cells. The experiments were repeated three times, and one of the representative was shown here. (* p
Figure Legend Snippet: WP1066, an STAT3-specific inhibitor, was used to clarify the role of STAT3 in immunosuppressive microenvironment. (A) (Left panel) Expressions of IDO, VEGF, IL-10, and CCL2/MCP-1 were assayed with Western blotting, and (right panel) their quantitative results. All proteins were suppressed after treated with WP1066. (B, C) Expressions of tomato fluorescent protein and intracellular IFN-γwere assayed by flow cytometry. Significantly higher tomato fluorescent protein and IFN-γsignals were found in CD8+ T cells co-cultured with sorafenib and WP1066-treated E.G7 cells, respectively. (D) Effect of WP1066 on migration of CD8+ T cells was evaluated with transwell assay. More migratory CD8+ T cells were found in WP1066-treated E.G7 cells. The experiments were repeated three times, and one of the representative was shown here. (* p

Techniques Used: Western Blot, Flow Cytometry, Cytometry, Cell Culture, Migration, Transwell Assay

7) Product Images from "Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages"

Article Title: Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages

Journal: Carcinogenesis

doi: 10.1093/carcin/bgw121

( A – C ) Six1 actives MAPK in vitro . ( A ) Western blots for MMP2, MMP9, VEGF, E-cadherin, vimentin, β-catenin, p-p38, p-JNK and p-ERK in two different isolates of MC38-Six1 and a MC38-Ctrl line. ( B ) Western blots for Six1, PCNA, cleaved caspase-3, E-cadherin, ALDH1, p-ERK and p-p38 in two different isolates of Six1-overexpressing HT29 (HT29-Six1) and SW480 (SW480-Six1) and corresponding controls (HT29-Ctrl and SW480-Ctrl). ( C ) Western blots for p-ERK, ERK, p-p38, p38 and E-cadherin in Six1-knockdown SW480 (SW480-shS1 and SW480-shS2), SW620 (SW620-shS1 and SW620-shS2), LoVo (LoVo-shS1 and LoVo-shS2) and SW48 (SW48-shS1 and SW48-shS2) as well as corresponding controls (SW480-shC, SW620-shC, LoVo-shC and SW48-shC). β-Actin was used as a loading control. ( D – I ) MC38 cells overexpressing Six1 recruit macrophages to tumors. ( D ) MC38-Six1 or MC38-Ctrl were injected into the flank of C57BL/6 mice and the mice killed 6 weeks later ( n = 9–10). The weight of tumors formed from MC38-Ctrl and MC38-Six1 is shown. ( E ) Peripheral white blood cell (WBC) count from MC38-Ctrl and MC38-Six1 tumor-bearing mice (cecal implantation). ( F ) Percentage of lymphocytes (LYM), monocytes (MON) and neutrophils (NEU) in peripheral WBC from MC38-Ctrl and MC38-Six1 tumor-bearing mice (cecal implantation). ( G ) Western blot of IL-1β, IL-6 and TNF-α in sera from MC38-Six1or MC38-Ctrl tumor-bearing mice (cecal implantation). ( H ) Left panels: Flow cytometry analysis of the expression of CD11b, F4/80 and Gr1 in MC38-Ctrl and MC38-Six1 tumors from the cecum. Right panels: the percentage of total cells positive for either CD11b + /F4/80 + (a marker for macrophages) or CD11b + /Gr1 + (a marker for neutrophils) cells. Results are representative of seven independent experiments. Bars indicate SD and *** indicates P
Figure Legend Snippet: ( A – C ) Six1 actives MAPK in vitro . ( A ) Western blots for MMP2, MMP9, VEGF, E-cadherin, vimentin, β-catenin, p-p38, p-JNK and p-ERK in two different isolates of MC38-Six1 and a MC38-Ctrl line. ( B ) Western blots for Six1, PCNA, cleaved caspase-3, E-cadherin, ALDH1, p-ERK and p-p38 in two different isolates of Six1-overexpressing HT29 (HT29-Six1) and SW480 (SW480-Six1) and corresponding controls (HT29-Ctrl and SW480-Ctrl). ( C ) Western blots for p-ERK, ERK, p-p38, p38 and E-cadherin in Six1-knockdown SW480 (SW480-shS1 and SW480-shS2), SW620 (SW620-shS1 and SW620-shS2), LoVo (LoVo-shS1 and LoVo-shS2) and SW48 (SW48-shS1 and SW48-shS2) as well as corresponding controls (SW480-shC, SW620-shC, LoVo-shC and SW48-shC). β-Actin was used as a loading control. ( D – I ) MC38 cells overexpressing Six1 recruit macrophages to tumors. ( D ) MC38-Six1 or MC38-Ctrl were injected into the flank of C57BL/6 mice and the mice killed 6 weeks later ( n = 9–10). The weight of tumors formed from MC38-Ctrl and MC38-Six1 is shown. ( E ) Peripheral white blood cell (WBC) count from MC38-Ctrl and MC38-Six1 tumor-bearing mice (cecal implantation). ( F ) Percentage of lymphocytes (LYM), monocytes (MON) and neutrophils (NEU) in peripheral WBC from MC38-Ctrl and MC38-Six1 tumor-bearing mice (cecal implantation). ( G ) Western blot of IL-1β, IL-6 and TNF-α in sera from MC38-Six1or MC38-Ctrl tumor-bearing mice (cecal implantation). ( H ) Left panels: Flow cytometry analysis of the expression of CD11b, F4/80 and Gr1 in MC38-Ctrl and MC38-Six1 tumors from the cecum. Right panels: the percentage of total cells positive for either CD11b + /F4/80 + (a marker for macrophages) or CD11b + /Gr1 + (a marker for neutrophils) cells. Results are representative of seven independent experiments. Bars indicate SD and *** indicates P

Techniques Used: In Vitro, Western Blot, Injection, Mouse Assay, Flow Cytometry, Cytometry, Expressing, Marker

Six1 overexpression promotes angiogenesis. ( A ) Upper panels: H E staining of primary tumors formed in the cecum of mice from MC38-Ctrl and MC38-Six1. Lower panels: immunofluorescent staining of CD31 (red) and α-SMA (red) merged with nuclei (blue) in MC38-Ctrl and MC38-Six1 tumors. ( B ) Western blots for VEGF, MMP9, MMP2 and LOX in sera from MC38-Six1 tumor-bearing mice and MC38-Ctrl mice. Albumin was used as a loading control. ( C ) The expression of MMP9, VEGF and LOX in MC38-Six1 and MC38-Ctrl tumors as assessed by immunohistochemistry (×400).
Figure Legend Snippet: Six1 overexpression promotes angiogenesis. ( A ) Upper panels: H E staining of primary tumors formed in the cecum of mice from MC38-Ctrl and MC38-Six1. Lower panels: immunofluorescent staining of CD31 (red) and α-SMA (red) merged with nuclei (blue) in MC38-Ctrl and MC38-Six1 tumors. ( B ) Western blots for VEGF, MMP9, MMP2 and LOX in sera from MC38-Six1 tumor-bearing mice and MC38-Ctrl mice. Albumin was used as a loading control. ( C ) The expression of MMP9, VEGF and LOX in MC38-Six1 and MC38-Ctrl tumors as assessed by immunohistochemistry (×400).

Techniques Used: Over Expression, Staining, Mouse Assay, Western Blot, Expressing, Immunohistochemistry

Six1 overexpression in MC38 increases the expression of molecules that induce chemotaxis of TAM. mRNA expression of CSF-1, CCL2, CCL5 and VEGF ( A ), CSF-2, CSF-3 and CXCL1 ( B ) and HIF-1α and HIF-1β ( C , upper panel) was determined by real-time PCR in MC38-Ctrl and MC38-Six1. Bars indicate SD, and ** and *** indicate P values
Figure Legend Snippet: Six1 overexpression in MC38 increases the expression of molecules that induce chemotaxis of TAM. mRNA expression of CSF-1, CCL2, CCL5 and VEGF ( A ), CSF-2, CSF-3 and CXCL1 ( B ) and HIF-1α and HIF-1β ( C , upper panel) was determined by real-time PCR in MC38-Ctrl and MC38-Six1. Bars indicate SD, and ** and *** indicate P values

Techniques Used: Over Expression, Expressing, Chemotaxis Assay, Real-time Polymerase Chain Reaction

8) Product Images from "RXRα provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells"

Article Title: RXRα provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0610-1

RXR overexpression in cancer cells inhibited proliferation, migration, and angiogenesis. a MTT assay and b EdU assay of MCF-7 transfected with RXRα after 48 h. c Flow cytometry detection of the cell cycle distribution of MCF-7 48 h after transfecting with RXRα. The migratory ability of MCF-7 overexpressing RXRα was determined via wound healing ( d ) and transwell chamber assays ( e ) as described in “Materials and methods”). The expression of Cyr61, Myl9, and MMP9 examined by qRT-PCR ( f ) and western blotting ( g ). h SA-β-galactosidase staining assay of parental and RXRα overexpression MCF-7 cells. i The expressions of ANGPTL3 and VEGF were examined by qRT-PCR ( j ) and western blotting ( k ) in MCF-7 overexpressing RXRα. Shown are the means ± SD from three independent experiments (* P
Figure Legend Snippet: RXR overexpression in cancer cells inhibited proliferation, migration, and angiogenesis. a MTT assay and b EdU assay of MCF-7 transfected with RXRα after 48 h. c Flow cytometry detection of the cell cycle distribution of MCF-7 48 h after transfecting with RXRα. The migratory ability of MCF-7 overexpressing RXRα was determined via wound healing ( d ) and transwell chamber assays ( e ) as described in “Materials and methods”). The expression of Cyr61, Myl9, and MMP9 examined by qRT-PCR ( f ) and western blotting ( g ). h SA-β-galactosidase staining assay of parental and RXRα overexpression MCF-7 cells. i The expressions of ANGPTL3 and VEGF were examined by qRT-PCR ( j ) and western blotting ( k ) in MCF-7 overexpressing RXRα. Shown are the means ± SD from three independent experiments (* P

Techniques Used: Over Expression, Migration, MTT Assay, EdU Assay, Transfection, Flow Cytometry, Cytometry, Expressing, Quantitative RT-PCR, Western Blot, Staining

9) Product Images from "Compound 49b Regulates ZO-1 and Occludin Levels in Human Retinal Endothelial Cells and in Mouse Retinal Vasculature"

Article Title: Compound 49b Regulates ZO-1 and Occludin Levels in Human Retinal Endothelial Cells and in Mouse Retinal Vasculature

Journal: Investigative Ophthalmology & Visual Science

doi: 10.1167/iovs.16-20412

Epac1 depletion increases VEGF expression and PKCzeta activation. Retinal endothelial cells were grown in NG, HG, HG + Compound 49b, HG + scrambled siRNA (HG + Sc), HG + Compound49b + scrambled siRNA (Sc + 49b), HG + Epac1 siRNA, or HG + Compound 49b + Epac1 siRNA (Epac1 siRNA + 49b). Panel A is a control to show Epac1 knockdown. Panel B is the ratio of phosphorylated PKCzeta to total PKCzeta. Panel C is VEGF levels compared with beta actin. N = 4 for each group of cells. * P
Figure Legend Snippet: Epac1 depletion increases VEGF expression and PKCzeta activation. Retinal endothelial cells were grown in NG, HG, HG + Compound 49b, HG + scrambled siRNA (HG + Sc), HG + Compound49b + scrambled siRNA (Sc + 49b), HG + Epac1 siRNA, or HG + Compound 49b + Epac1 siRNA (Epac1 siRNA + 49b). Panel A is a control to show Epac1 knockdown. Panel B is the ratio of phosphorylated PKCzeta to total PKCzeta. Panel C is VEGF levels compared with beta actin. N = 4 for each group of cells. * P

Techniques Used: Expressing, Activation Assay

Compound 49b requires Epac1 to decrease permeability. Panel A is a bar graph of the diffusive flux on REC grown in normal glucose (NG) or high glucose (HG) or HG + 50 nM Compound 49b or 10 μM VEGF. N = 4 for each group. * P
Figure Legend Snippet: Compound 49b requires Epac1 to decrease permeability. Panel A is a bar graph of the diffusive flux on REC grown in normal glucose (NG) or high glucose (HG) or HG + 50 nM Compound 49b or 10 μM VEGF. N = 4 for each group. * P

Techniques Used: Permeability

10) Product Images from "Paired box 5 is a novel marker of breast cancers that is frequently downregulated by methylation"

Article Title: Paired box 5 is a novel marker of breast cancers that is frequently downregulated by methylation

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.27599

PAX5 involved in the regulation of cell cycle pathway and VEGF expression. (A) Western-blot is performed to test the effect of PAX5 on cell cycle pathway and the expression of VEGF. (B) It is shown that PAX5 increases the expression of p53, p21, p27 and decreases the expression of cyclin D1, CDK4, VEGF in breast cancer cells (BT549 and MB231). The values are exhibited as the mean ± SD from three independent experiments (**, p
Figure Legend Snippet: PAX5 involved in the regulation of cell cycle pathway and VEGF expression. (A) Western-blot is performed to test the effect of PAX5 on cell cycle pathway and the expression of VEGF. (B) It is shown that PAX5 increases the expression of p53, p21, p27 and decreases the expression of cyclin D1, CDK4, VEGF in breast cancer cells (BT549 and MB231). The values are exhibited as the mean ± SD from three independent experiments (**, p

Techniques Used: Expressing, Western Blot

11) Product Images from "Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer"

Article Title: Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2018/3510970

Melatonin hampered oral cancer tumorigenesis in vivo . SCID mice were subcutaneously injected with 2 × 10 6 Cal27 cells. After 7 days, the animals received intraperitoneally melatonin or the vehicle (control) five days a week in a span of three weeks. All the mice were sacrificed under euthanasia six weeks after tumor cell implantation. (a) Representative images of tumors from the two groups. (b) Tumor volume was measured and calculated once a week for six weeks. (c) Tumor weight was measured. (d) ROS level was measured in the tumor tissues. (e) Western blot results of p-Akt, Akt, p-ERK, ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1 α , and VEGF in the tumor tissues. GAPDH was used as endogenous control. The ratios from the indicated proteins to GAPDH are indicated below the bands. (f) IHC assays were performed to evaluate the levels of p-Akt, p-ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1 α , and VEGF in the tumor tissues. Data are represented as the mean ± SD of three independent experiments. ∗ P
Figure Legend Snippet: Melatonin hampered oral cancer tumorigenesis in vivo . SCID mice were subcutaneously injected with 2 × 10 6 Cal27 cells. After 7 days, the animals received intraperitoneally melatonin or the vehicle (control) five days a week in a span of three weeks. All the mice were sacrificed under euthanasia six weeks after tumor cell implantation. (a) Representative images of tumors from the two groups. (b) Tumor volume was measured and calculated once a week for six weeks. (c) Tumor weight was measured. (d) ROS level was measured in the tumor tissues. (e) Western blot results of p-Akt, Akt, p-ERK, ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1 α , and VEGF in the tumor tissues. GAPDH was used as endogenous control. The ratios from the indicated proteins to GAPDH are indicated below the bands. (f) IHC assays were performed to evaluate the levels of p-Akt, p-ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1 α , and VEGF in the tumor tissues. Data are represented as the mean ± SD of three independent experiments. ∗ P

Techniques Used: In Vivo, Mouse Assay, Injection, Western Blot, Immunohistochemistry

12) Product Images from "Enhanced cytotoxicity of human hepatocellular carcinoma cells following pretreatment with sorafenib combined with trichostatin A"

Article Title: Enhanced cytotoxicity of human hepatocellular carcinoma cells following pretreatment with sorafenib combined with trichostatin A

Journal: Oncology Letters

doi: 10.3892/ol.2018.9582

Effects of TSA treatment on cell viability, NF-κB activity and its downstream effector proteins in Huh7/NF-κB- luc2 cells. (A) The cytotoxicity of TSA was determined using an MTT assay. (B) NF-κB activity was determined by bioluminescence imaging using NF-κB as the promoter and luciferase gene as the reporter. (C) Cells were treated with TSA (1 µM) for 0 h (control) and 48 h, respectively. The expression of NF-κB downstream effector proteins including VEGF, MMP-9, XIAP and Bcl-2 was assessed by western blotting. *P
Figure Legend Snippet: Effects of TSA treatment on cell viability, NF-κB activity and its downstream effector proteins in Huh7/NF-κB- luc2 cells. (A) The cytotoxicity of TSA was determined using an MTT assay. (B) NF-κB activity was determined by bioluminescence imaging using NF-κB as the promoter and luciferase gene as the reporter. (C) Cells were treated with TSA (1 µM) for 0 h (control) and 48 h, respectively. The expression of NF-κB downstream effector proteins including VEGF, MMP-9, XIAP and Bcl-2 was assessed by western blotting. *P

Techniques Used: Activity Assay, MTT Assay, Imaging, Luciferase, Expressing, Western Blot

13) Product Images from "FBXL19-AS1 exerts oncogenic function by sponging miR-431-5p to regulate RAF1 expression in lung cancer"

Article Title: FBXL19-AS1 exerts oncogenic function by sponging miR-431-5p to regulate RAF1 expression in lung cancer

Journal: Bioscience Reports

doi: 10.1042/BSR20181804

FBXL19-AS1 knockdown inhibits proliferation, migration and invasion, and reduces the expression levels of angiogenesis related proteins in lung cancer cells ( A ) The knockdown efficiency of FBXL19-AS1 in A549 and H1299 cells was examined by RT-qPCR. ( B ) At the indicated time points (24, 48, 72 and 96 h), the proliferation of transfected cells was determined by CCK8 assay. ( C ) After 2 weeks of transfection, colony formation assay was performed. ( D and E ) Transwell assay presented that the knockdown of FBXL19-AS1 inhibits migration and invasion in A549 and H1299 cells. ( F ) After 48 h of transfection, protein expressions of VEGF, Ang1, and FGF2 were measured by Western blot assay. Error bars represent the mean ± SD of at least three independent experiments. ** P
Figure Legend Snippet: FBXL19-AS1 knockdown inhibits proliferation, migration and invasion, and reduces the expression levels of angiogenesis related proteins in lung cancer cells ( A ) The knockdown efficiency of FBXL19-AS1 in A549 and H1299 cells was examined by RT-qPCR. ( B ) At the indicated time points (24, 48, 72 and 96 h), the proliferation of transfected cells was determined by CCK8 assay. ( C ) After 2 weeks of transfection, colony formation assay was performed. ( D and E ) Transwell assay presented that the knockdown of FBXL19-AS1 inhibits migration and invasion in A549 and H1299 cells. ( F ) After 48 h of transfection, protein expressions of VEGF, Ang1, and FGF2 were measured by Western blot assay. Error bars represent the mean ± SD of at least three independent experiments. ** P

Techniques Used: Migration, Expressing, Quantitative RT-PCR, Transfection, CCK-8 Assay, Colony Assay, Transwell Assay, Western Blot

Overexpression of RAF1 weakens FBXL19-AS1 knockdown-mediated inhibition of lung cancer progression ( A ) RT-qPCR results showed that down-expression of FBXL19-AS1 reduced the expression of RAF1. ( B ) CCK8 assay implied that decreased FBXL19-AS1 expression inhibited cell proliferation in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cell proliferation. ( C ) Colony formation assay further implied that decreased FBXL19-AS1 expression inhibited cell proliferation in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cell proliferation. ( D and E ) Transwell assay presented that decreased FBXL19-AS1 expression inhibited cells migration and invasion in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cells migration and invasion. ( F ) Western blot assay presented that decreased FBXL19-AS1 expression inhibited protein expressions of VEGF, Ang1, and FGF2 in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of protein expressions (VEGF, Ang1, and FGF2). Error bars represent the mean ± SD of at least three independent experiments. * P
Figure Legend Snippet: Overexpression of RAF1 weakens FBXL19-AS1 knockdown-mediated inhibition of lung cancer progression ( A ) RT-qPCR results showed that down-expression of FBXL19-AS1 reduced the expression of RAF1. ( B ) CCK8 assay implied that decreased FBXL19-AS1 expression inhibited cell proliferation in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cell proliferation. ( C ) Colony formation assay further implied that decreased FBXL19-AS1 expression inhibited cell proliferation in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cell proliferation. ( D and E ) Transwell assay presented that decreased FBXL19-AS1 expression inhibited cells migration and invasion in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of cells migration and invasion. ( F ) Western blot assay presented that decreased FBXL19-AS1 expression inhibited protein expressions of VEGF, Ang1, and FGF2 in A549 and H1299 cells. However, overexpression of RAF1 weakened FBXL19-AS1 knockdown-mediated inhibition of protein expressions (VEGF, Ang1, and FGF2). Error bars represent the mean ± SD of at least three independent experiments. * P

Techniques Used: Over Expression, Inhibition, Quantitative RT-PCR, Expressing, CCK-8 Assay, Colony Assay, Transwell Assay, Migration, Western Blot

14) Product Images from "Combined Preconditioning and Postconditioning Provides Synergistic Protection against Liver Ischemic Reperfusion Injury"

Article Title: Combined Preconditioning and Postconditioning Provides Synergistic Protection against Liver Ischemic Reperfusion Injury

Journal: International Journal of Biological Sciences

doi: 10.7150/ijbs.4231

Effect of pre- and postconditioning on the expression level of HIF-1 alpha, PHD and VEGF. Whole cell extracts made from mouse liver were separated on SDS- page gel. HIF-1 α , PHD, VEGF and GAPDH protein level were determined by immunblotting with the specific antibodies against the proteins listed on the right. GAPDH was used as a loading control. Effect of GSP on the expression level of HIF-1 alpha, PHD and VEGF. (mean ±s, n=7). HIF-1 α , PHD, VEGF and GAPDH mRNA level were determined by Real-Time PCR. (* indicate P
Figure Legend Snippet: Effect of pre- and postconditioning on the expression level of HIF-1 alpha, PHD and VEGF. Whole cell extracts made from mouse liver were separated on SDS- page gel. HIF-1 α , PHD, VEGF and GAPDH protein level were determined by immunblotting with the specific antibodies against the proteins listed on the right. GAPDH was used as a loading control. Effect of GSP on the expression level of HIF-1 alpha, PHD and VEGF. (mean ±s, n=7). HIF-1 α , PHD, VEGF and GAPDH mRNA level were determined by Real-Time PCR. (* indicate P

Techniques Used: Expressing, SDS Page, Real-time Polymerase Chain Reaction

15) Product Images from "Secreted Protein Acidic and Rich in Cysteine (SPARC) Suppresses Angiogenesis by Down-Regulating the Expression of VEGF and MMP-7 in Gastric Cancer"

Article Title: Secreted Protein Acidic and Rich in Cysteine (SPARC) Suppresses Angiogenesis by Down-Regulating the Expression of VEGF and MMP-7 in Gastric Cancer

Journal: PLoS ONE

doi: 10.1371/journal.pone.0044618

The MAPKs signalling pathway and expression of VEGF and MMP-7 are decreased by SPARC overexpression. ( A ) Cell lysates were used to perform western blotting analysis for VEGF and MMP-7 expression. GAPDH served as loading control. The expressions of VEGF and MMP-7 were declined at protein level in BGC-SP cells. The expressions of VEGF and MMP-7 were increased at protein level in HGC-sh cells. Columns are means (±s.d.) of triplicate experiments; *P
Figure Legend Snippet: The MAPKs signalling pathway and expression of VEGF and MMP-7 are decreased by SPARC overexpression. ( A ) Cell lysates were used to perform western blotting analysis for VEGF and MMP-7 expression. GAPDH served as loading control. The expressions of VEGF and MMP-7 were declined at protein level in BGC-SP cells. The expressions of VEGF and MMP-7 were increased at protein level in HGC-sh cells. Columns are means (±s.d.) of triplicate experiments; *P

Techniques Used: Expressing, Over Expression, Western Blot

Overexpression of SPARC in gastric cancer cells inhibits tumour development and vascularisation in nude mice. ( A ) Paraffin-embedded sections of xenografted tumours were used for immunohistochemical analysis of SPARC, MMP-7, VEGF, and CD-31. ( B ) Sections were stained with a monoclonal antibody against human SPARC, VEGF, MMP-7. Sum densities were calculated and analyzed by IPP 6.0. Columns are means (±s.d.) of quadruplicate determinations from six mice in each group. *P
Figure Legend Snippet: Overexpression of SPARC in gastric cancer cells inhibits tumour development and vascularisation in nude mice. ( A ) Paraffin-embedded sections of xenografted tumours were used for immunohistochemical analysis of SPARC, MMP-7, VEGF, and CD-31. ( B ) Sections were stained with a monoclonal antibody against human SPARC, VEGF, MMP-7. Sum densities were calculated and analyzed by IPP 6.0. Columns are means (±s.d.) of quadruplicate determinations from six mice in each group. *P

Techniques Used: Over Expression, Mouse Assay, Immunohistochemistry, Staining

Knock-down of SPARC expression in HGC-27 cells promotes angiogenesis via up-regulated VEGF and MMP-7 expression. ( A ) Conditioned media from HGC-P, HGC-EV, HGC-sh with or without rhSPARC (0.3 µg/ml) and HGC-sh+MMP7-sh cells were concentrated under the same conditions. β-casein zymography was conducted for MMP-7 activity. Western blotting analysis was performed for MMP-7, SPARC and VEGF protein levels in conditioned media. The cells were collected and lysates probed with GAPDH antibody to calibrate total amount of the respective proteins. Columns are means (±s.d.) of triplicate experiments. ( B ) In vitro angiogenesis: To confirm that SPARC expression-mediated anti-angiogenic effects are due to altered MMP-7 and VEGF expression rather than to the expression of SPARC itself, harvested supernatant from HGC-sh cells was added to 0.3 µg/ml rhSPARC. Supernatants from both of HGC-sh and HGC-sh+MMP7-sh cells with neutralising antibody to VEGF were also used in co-culture assay (anti-VEGF = neutralising antibody to VEGF). HUVECs were seeded in Matrigel-coated 96-well plates incubated with conditioned media. The effects of conditioned media on the pre-formed tubes of HUVECs were analysed, and the tube length was measured. Tube length data shown are the means (±s.d.) of quadruplicate determinations from three separate experiments. *P
Figure Legend Snippet: Knock-down of SPARC expression in HGC-27 cells promotes angiogenesis via up-regulated VEGF and MMP-7 expression. ( A ) Conditioned media from HGC-P, HGC-EV, HGC-sh with or without rhSPARC (0.3 µg/ml) and HGC-sh+MMP7-sh cells were concentrated under the same conditions. β-casein zymography was conducted for MMP-7 activity. Western blotting analysis was performed for MMP-7, SPARC and VEGF protein levels in conditioned media. The cells were collected and lysates probed with GAPDH antibody to calibrate total amount of the respective proteins. Columns are means (±s.d.) of triplicate experiments. ( B ) In vitro angiogenesis: To confirm that SPARC expression-mediated anti-angiogenic effects are due to altered MMP-7 and VEGF expression rather than to the expression of SPARC itself, harvested supernatant from HGC-sh cells was added to 0.3 µg/ml rhSPARC. Supernatants from both of HGC-sh and HGC-sh+MMP7-sh cells with neutralising antibody to VEGF were also used in co-culture assay (anti-VEGF = neutralising antibody to VEGF). HUVECs were seeded in Matrigel-coated 96-well plates incubated with conditioned media. The effects of conditioned media on the pre-formed tubes of HUVECs were analysed, and the tube length was measured. Tube length data shown are the means (±s.d.) of quadruplicate determinations from three separate experiments. *P

Techniques Used: Expressing, Zymography, Activity Assay, Western Blot, In Vitro, Co-culture Assay, Incubation

16) Product Images from "Anti-Angiogenic and Anti-Inflammatory Effects of SERPINA3K on Corneal Injury"

Article Title: Anti-Angiogenic and Anti-Inflammatory Effects of SERPINA3K on Corneal Injury

Journal: PLoS ONE

doi: 10.1371/journal.pone.0016712

Down-regulation of anti-angiogenic and anti-inflammatory factors by SERPINA3K. ( A ) Western blotting results of VEGF and PEDF on day 8 after alkali burn. Individual lanes from left to right, 1 2: control group, without alkali burn; 3 4: alkali burn with PBS treatment; 5 6: alkali burn with BSA treatment; 7–8: alkali burn with SERPINA3K (SA3K) treatment (20 µg/eye/day). ( B ) The statistic analysis of Western blotting results of VEGF between the groups on day 8 (Data are presented as Mean±SEM, n = 3 in each group). The level of VEGF was significantly reduced in the SERPINA3K-treated group, compared to the BSA-treated group. ( C ) The statistic analysis of Western blotting results of PEDF between the groups (data are presented as Mean±SEM, n = 3 in each group) on day 8. The level of PEDF was significantly up-regulated in the SERPINA3K-treated group, compared to the BSA-treated group. ( D ) The Western blotting results of TNF-α on day 8 after alkali burn. The order of individual lanes was as same as ( A ). ( E ) The statistic analysis of Western blotting results of TNF-α between the groups on day 8 (data are presented as Mean±SEM, n = 3 in each group). The level of TNF-α was significantly reduced in the SERPINA3K-treated group, compared to the BSA-treated group. ( F ) The effects of SERPINA3K on the cell viability of HCE cells and HUVEC by the MTT assay (data are presented as Mean±SEM, n = 5 in each group). It showed the inhibitory effect of SERPINA3K on the cell viability of HUVEC, but not HCE cells at the concentrations given. (* p
Figure Legend Snippet: Down-regulation of anti-angiogenic and anti-inflammatory factors by SERPINA3K. ( A ) Western blotting results of VEGF and PEDF on day 8 after alkali burn. Individual lanes from left to right, 1 2: control group, without alkali burn; 3 4: alkali burn with PBS treatment; 5 6: alkali burn with BSA treatment; 7–8: alkali burn with SERPINA3K (SA3K) treatment (20 µg/eye/day). ( B ) The statistic analysis of Western blotting results of VEGF between the groups on day 8 (Data are presented as Mean±SEM, n = 3 in each group). The level of VEGF was significantly reduced in the SERPINA3K-treated group, compared to the BSA-treated group. ( C ) The statistic analysis of Western blotting results of PEDF between the groups (data are presented as Mean±SEM, n = 3 in each group) on day 8. The level of PEDF was significantly up-regulated in the SERPINA3K-treated group, compared to the BSA-treated group. ( D ) The Western blotting results of TNF-α on day 8 after alkali burn. The order of individual lanes was as same as ( A ). ( E ) The statistic analysis of Western blotting results of TNF-α between the groups on day 8 (data are presented as Mean±SEM, n = 3 in each group). The level of TNF-α was significantly reduced in the SERPINA3K-treated group, compared to the BSA-treated group. ( F ) The effects of SERPINA3K on the cell viability of HCE cells and HUVEC by the MTT assay (data are presented as Mean±SEM, n = 5 in each group). It showed the inhibitory effect of SERPINA3K on the cell viability of HUVEC, but not HCE cells at the concentrations given. (* p

Techniques Used: Western Blot, MTT Assay

17) Product Images from "Combined application of anti-VEGF and anti-EGFR attenuates the growth and angiogenesis of colorectal cancer mainly through suppressing AKT and ERK signaling in mice model"

Article Title: Combined application of anti-VEGF and anti-EGFR attenuates the growth and angiogenesis of colorectal cancer mainly through suppressing AKT and ERK signaling in mice model

Journal: BMC Cancer

doi: 10.1186/s12885-016-2834-8

Suppression of CRC cells tumor angiogenesis by anti-VEGF and anti-EGFR antibodies. a Representative photographs of anti-CD34 staining in SW620 cells tumors. b The numbers of positively CD34 stained cells in subcutaneous SW620 and LoVo cells tumors. The data are representative of at least three different experiments ± SEM. * P
Figure Legend Snippet: Suppression of CRC cells tumor angiogenesis by anti-VEGF and anti-EGFR antibodies. a Representative photographs of anti-CD34 staining in SW620 cells tumors. b The numbers of positively CD34 stained cells in subcutaneous SW620 and LoVo cells tumors. The data are representative of at least three different experiments ± SEM. * P

Techniques Used: Staining

Combined application of anti-VEGF and anti-EGFR antibodies attenuates the activation of AKT and ERK, but not STAT3, c-Myc and NF-κB in vivo. a Western blot analysis was performed to determine the activation of AKT, ERK1/2 and STAT3 in different SW620 cells tumors. b Western blot assay of different LoVo cells tumors (one clone, a ). c Western blot analysis was performed to determine the activation of c-Myc, NF-κB/p65 and IκBα in different SW620 cells tumors. d Western blot assay of different LoVo cells tumors (one clone, c )
Figure Legend Snippet: Combined application of anti-VEGF and anti-EGFR antibodies attenuates the activation of AKT and ERK, but not STAT3, c-Myc and NF-κB in vivo. a Western blot analysis was performed to determine the activation of AKT, ERK1/2 and STAT3 in different SW620 cells tumors. b Western blot assay of different LoVo cells tumors (one clone, a ). c Western blot analysis was performed to determine the activation of c-Myc, NF-κB/p65 and IκBα in different SW620 cells tumors. d Western blot assay of different LoVo cells tumors (one clone, c )

Techniques Used: Activation Assay, In Vivo, Western Blot

VEGF and EGFR expression are significantly upregulated in liver-metastatic CRC tissues. a Results of VEGF staining were evaluated by the staining scores. b Results of EGFR staining were evaluated by the staining scores. c Immunohistochemistry analysis of VEGF and EGFR expression in different colorectal tissues. * P
Figure Legend Snippet: VEGF and EGFR expression are significantly upregulated in liver-metastatic CRC tissues. a Results of VEGF staining were evaluated by the staining scores. b Results of EGFR staining were evaluated by the staining scores. c Immunohistochemistry analysis of VEGF and EGFR expression in different colorectal tissues. * P

Techniques Used: Expressing, Staining, Immunohistochemistry

Expression of VEGF and EGFR in CRC cell lines. a Expression of VEGF in four human CRC cell lines was detected by qRT-PCR. b Expression of EGFR in four human CRC cell lines was detected by qRT-PCR. c Western blot analysis of VEGF and EGFR expression in different CRC cell lines
Figure Legend Snippet: Expression of VEGF and EGFR in CRC cell lines. a Expression of VEGF in four human CRC cell lines was detected by qRT-PCR. b Expression of EGFR in four human CRC cell lines was detected by qRT-PCR. c Western blot analysis of VEGF and EGFR expression in different CRC cell lines

Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

Suppression of CRC cells tumorigenicity by anti-VEGF and anti-EGFR antibodies in vivo. a Representative photographs of tumor formation in mice in response to SW620 cells. b Five weeks later, the tumors were resected and weighted. The weight analyzed with Student’s t -test. Data represent means ± SEM. * P
Figure Legend Snippet: Suppression of CRC cells tumorigenicity by anti-VEGF and anti-EGFR antibodies in vivo. a Representative photographs of tumor formation in mice in response to SW620 cells. b Five weeks later, the tumors were resected and weighted. The weight analyzed with Student’s t -test. Data represent means ± SEM. * P

Techniques Used: In Vivo, Mouse Assay

Combined application of anti-VEGF and anti-EGFR antibodies suppresses the proliferation and invasion of CRC cells in vitro. a The proliferation rate of SW620 and LoVo cells were analyzed by CCK-8 assay in different groups. b Invasion assay of SW620 and LoVo cells in different groups. c Invasion of SW620 and LoVo cells were quantitatively analyzed in different groups. Columns are the average of three independent experiments ± SEM. * P
Figure Legend Snippet: Combined application of anti-VEGF and anti-EGFR antibodies suppresses the proliferation and invasion of CRC cells in vitro. a The proliferation rate of SW620 and LoVo cells were analyzed by CCK-8 assay in different groups. b Invasion assay of SW620 and LoVo cells in different groups. c Invasion of SW620 and LoVo cells were quantitatively analyzed in different groups. Columns are the average of three independent experiments ± SEM. * P

Techniques Used: In Vitro, CCK-8 Assay, Invasion Assay

18) Product Images from "Vascular Endothelial Growth Factor and Cluster of Differentiation 34 for Assessment of Perioperative Bleeding Risk in Gastric Cancer Patients"

Article Title: Vascular Endothelial Growth Factor and Cluster of Differentiation 34 for Assessment of Perioperative Bleeding Risk in Gastric Cancer Patients

Journal: Chinese Medical Journal

doi: 10.4103/0366-6999.187842

Expression of CD34 and VEGF in perioperative hemorrhage in gastric cancer patients and normal individuals via immunohistochemical staining. Expression of CD34 (a and c) in normal tissue and gastric cancer tissue, respectively; and expression of VEGF (b and d) in normal tissue and gastric cancer tissue, respectively (original magnification, ×200). VEGF: Vascular endothelial growth factor; CD34: Cluster of differentiation 34.
Figure Legend Snippet: Expression of CD34 and VEGF in perioperative hemorrhage in gastric cancer patients and normal individuals via immunohistochemical staining. Expression of CD34 (a and c) in normal tissue and gastric cancer tissue, respectively; and expression of VEGF (b and d) in normal tissue and gastric cancer tissue, respectively (original magnification, ×200). VEGF: Vascular endothelial growth factor; CD34: Cluster of differentiation 34.

Techniques Used: Expressing, Immunohistochemistry, Staining

19) Product Images from "hTERT promotes tumor angiogenesis by activating VEGF via interactions with the Sp1 transcription factor"

Article Title: hTERT promotes tumor angiogenesis by activating VEGF via interactions with the Sp1 transcription factor

Journal: Nucleic Acids Research

doi: 10.1093/nar/gkw549

hTERT up-regulates VEGF expression in HeLa cells through Sp1 activity. ( A ) HeLa cells were transduced with lentiviruses expressing hTERT, K626A and GFP as a control. At 48 h after infection, VEGF mRNA levels were quantified by qPCR. ( B ) The protein levels of VEGF, hTERT and Actin were determined by immunoblotting. ( C ) Quantitative expression of VEGF from three independent experiments was analyzed using Quantity One 1-D Analysis Software and normalized to Actin levels. ( D and E ) HeLa cells were transiently transfected with pcDNA3-hTERT (hTERT) and pcDNA3 as a control, along with luciferase reporter plasmids containing different regions of the VEGF promoter or mutations in two or all three Sp1 binding sites. Luciferase activity was determined at 48 h after transfection. ( F and G ) Knockdown of Sp1 decreased the endogenous levels of VEGF mRNA. HeLa-GFP and HeLa-hTERT stable cells were transfected with control siRNA (siNC) or siRNA (mix) against Sp1. The mRNA levels of VEGF were analyzed by qPCR, and the levels of hTERT and Sp1 protein expression were determined by Western blot analysis using hTERT and Sp1 antibodies. ( H ) HeLa-GFP and HeLa-hTERT stable cells were treated with MTA (100 nM), PDTC (100 μM) or DMSO for an additional 24 h. VEGF mRNA levels were quantified by qPCR. The data are presented as the mean ± S.D. (Student's t -test). * P
Figure Legend Snippet: hTERT up-regulates VEGF expression in HeLa cells through Sp1 activity. ( A ) HeLa cells were transduced with lentiviruses expressing hTERT, K626A and GFP as a control. At 48 h after infection, VEGF mRNA levels were quantified by qPCR. ( B ) The protein levels of VEGF, hTERT and Actin were determined by immunoblotting. ( C ) Quantitative expression of VEGF from three independent experiments was analyzed using Quantity One 1-D Analysis Software and normalized to Actin levels. ( D and E ) HeLa cells were transiently transfected with pcDNA3-hTERT (hTERT) and pcDNA3 as a control, along with luciferase reporter plasmids containing different regions of the VEGF promoter or mutations in two or all three Sp1 binding sites. Luciferase activity was determined at 48 h after transfection. ( F and G ) Knockdown of Sp1 decreased the endogenous levels of VEGF mRNA. HeLa-GFP and HeLa-hTERT stable cells were transfected with control siRNA (siNC) or siRNA (mix) against Sp1. The mRNA levels of VEGF were analyzed by qPCR, and the levels of hTERT and Sp1 protein expression were determined by Western blot analysis using hTERT and Sp1 antibodies. ( H ) HeLa-GFP and HeLa-hTERT stable cells were treated with MTA (100 nM), PDTC (100 μM) or DMSO for an additional 24 h. VEGF mRNA levels were quantified by qPCR. The data are presented as the mean ± S.D. (Student's t -test). * P

Techniques Used: Expressing, Activity Assay, Transduction, Infection, Real-time Polymerase Chain Reaction, Software, Transfection, Luciferase, Binding Assay, Western Blot

hTERT binds to the VEGF promoter. ( A and B ) HeLa cell nuclear extracts were prepared 48 h after cells were transfected with hTERT expression vectors. EMSA supershift analyses using the (A) synthetic consensus Sp1 probe or the VEGF probe containing ( B ) three Sp1 binding sites were performed via the addition of specific hTERT or Sp1 antibodies. ( C ) HeLa cells were transfected with vectors expressing Flag-hTERT, and ChIP assays were performed using the Flag antibody and Sp1 antibody. IgG was used as the negative control. The signal enrichment with each antibody was measured by PCR using primers specific for VEGF or GAPDH as the negative control. The data shown are representative of two independent experiments. ( D ) HeLa cells were transiently transfected with the indicated vectors, along with the luciferase reporter pSp1-luc or pLG6-TA as a control. ( E ) siTERT or control siRNA was transfected into HeLa cells, along with pSp1-luc. Luciferase activity was determined 48 h after transfection. ( F ) The knockdown efficiency of hTERT expression by hTERT siRNAs was evaluated by qPCR analysis.
Figure Legend Snippet: hTERT binds to the VEGF promoter. ( A and B ) HeLa cell nuclear extracts were prepared 48 h after cells were transfected with hTERT expression vectors. EMSA supershift analyses using the (A) synthetic consensus Sp1 probe or the VEGF probe containing ( B ) three Sp1 binding sites were performed via the addition of specific hTERT or Sp1 antibodies. ( C ) HeLa cells were transfected with vectors expressing Flag-hTERT, and ChIP assays were performed using the Flag antibody and Sp1 antibody. IgG was used as the negative control. The signal enrichment with each antibody was measured by PCR using primers specific for VEGF or GAPDH as the negative control. The data shown are representative of two independent experiments. ( D ) HeLa cells were transiently transfected with the indicated vectors, along with the luciferase reporter pSp1-luc or pLG6-TA as a control. ( E ) siTERT or control siRNA was transfected into HeLa cells, along with pSp1-luc. Luciferase activity was determined 48 h after transfection. ( F ) The knockdown efficiency of hTERT expression by hTERT siRNAs was evaluated by qPCR analysis.

Techniques Used: Transfection, Expressing, Binding Assay, Chromatin Immunoprecipitation, Negative Control, Polymerase Chain Reaction, Luciferase, Activity Assay, Real-time Polymerase Chain Reaction

hTERT expression correlates with VEGF and CD31 in gastric tumors. ( A and B ) qRT-PCR analysis of (A) VEGF , (B) CD31 and hTERT expression in 23 human gastric mucosa tissues. ( C ) Regression analysis of the correlation between VEGF and hTERT expression. ( D ) Regression analysis of the correlation between CD31 and hTERT expression. Each point represents one cancer sample.
Figure Legend Snippet: hTERT expression correlates with VEGF and CD31 in gastric tumors. ( A and B ) qRT-PCR analysis of (A) VEGF , (B) CD31 and hTERT expression in 23 human gastric mucosa tissues. ( C ) Regression analysis of the correlation between VEGF and hTERT expression. ( D ) Regression analysis of the correlation between CD31 and hTERT expression. Each point represents one cancer sample.

Techniques Used: Expressing, Quantitative RT-PCR

20) Product Images from "A novel IL-1RA-PEP fusion protein alleviates blood-brain barrier disruption after ischemia-reperfusion in male rats"

Article Title: A novel IL-1RA-PEP fusion protein alleviates blood-brain barrier disruption after ischemia-reperfusion in male rats

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-018-1058-z

Role of p65/NF-κB pathways in IL-1RA-PEP-mediated effects on blood-brain barrier (BBB) disruption. a After the JSH-23 inhibitor was administered, expression levels of ZO-1, MMP-9, angiopoietin-1, and VEGF were analyzed by western blot in the different groups. b–e The gray value of the band was scanned by optical densitometry, and the ratio value was statistically analyzed. Data are shown as mean ± SEM; * P
Figure Legend Snippet: Role of p65/NF-κB pathways in IL-1RA-PEP-mediated effects on blood-brain barrier (BBB) disruption. a After the JSH-23 inhibitor was administered, expression levels of ZO-1, MMP-9, angiopoietin-1, and VEGF were analyzed by western blot in the different groups. b–e The gray value of the band was scanned by optical densitometry, and the ratio value was statistically analyzed. Data are shown as mean ± SEM; * P

Techniques Used: Expressing, Western Blot

21) Product Images from "SSRP1 silencing inhibits the proliferation and malignancy of human glioma cells via the MAPK signaling pathway"

Article Title: SSRP1 silencing inhibits the proliferation and malignancy of human glioma cells via the MAPK signaling pathway

Journal: Oncology Reports

doi: 10.3892/or.2017.5982

Structure-specific recognition protein 1 (SSRP1) regulates the expression of proliferation- and migration-associated genes in glioma via the MAPK pathway. (A and B) Knockdown of SSRP1 expression decreased the expression of proliferation-associated genes, including p65, c-myc, cyclin D and E. The expression of EGFR, VEGF and Snail, proteins involved in migration, were also suppressed. (C and D) The downregulated expression of SSRP1 significantly decreased the total and phosphorylated protein levels of p38 and ERK, and only the phosphorylated protein levels of JNK.
Figure Legend Snippet: Structure-specific recognition protein 1 (SSRP1) regulates the expression of proliferation- and migration-associated genes in glioma via the MAPK pathway. (A and B) Knockdown of SSRP1 expression decreased the expression of proliferation-associated genes, including p65, c-myc, cyclin D and E. The expression of EGFR, VEGF and Snail, proteins involved in migration, were also suppressed. (C and D) The downregulated expression of SSRP1 significantly decreased the total and phosphorylated protein levels of p38 and ERK, and only the phosphorylated protein levels of JNK.

Techniques Used: Expressing, Migration

22) Product Images from "Serum-derived carcinoembryonic antigen (CEA) activates fibroblasts to induce a local re-modeling of the extracellular matrix that favors the engraftment of CEA-expressing tumor cells"

Article Title: Serum-derived carcinoembryonic antigen (CEA) activates fibroblasts to induce a local re-modeling of the extracellular matrix that favors the engraftment of CEA-expressing tumor cells

Journal: International journal of cancer

doi: 10.1002/ijc.31586

Affinity-purified serum CEA (sCEA) derived from cancer patients activates naïve human neonatal fibroblasts (HNNFbs). A. sCEA induces changes of fibroblast cellular morphology. Photomicrograph of semi-confluent HNNFb cultures stimulated by TGF-β (5pg/mL), sCEA or BSA (200 ng/mL) for 24 hours. Note the change in cellular morphology of TGF-β and sCEA treated HNNFb cultures. B. Fluorescence images of untreated and sCEA-treated HNNFbs stained with FITC-phalloidin. C. Stimulation of HNNFbs with sCEA triggers an increase in paxillin phosphorylation. D. Activation of HNNFbs with sCEA results in the upregulation of α-SMA and VEGF expression.
Figure Legend Snippet: Affinity-purified serum CEA (sCEA) derived from cancer patients activates naïve human neonatal fibroblasts (HNNFbs). A. sCEA induces changes of fibroblast cellular morphology. Photomicrograph of semi-confluent HNNFb cultures stimulated by TGF-β (5pg/mL), sCEA or BSA (200 ng/mL) for 24 hours. Note the change in cellular morphology of TGF-β and sCEA treated HNNFb cultures. B. Fluorescence images of untreated and sCEA-treated HNNFbs stained with FITC-phalloidin. C. Stimulation of HNNFbs with sCEA triggers an increase in paxillin phosphorylation. D. Activation of HNNFbs with sCEA results in the upregulation of α-SMA and VEGF expression.

Techniques Used: Affinity Purification, Derivative Assay, Fluorescence, Staining, Activation Assay, Expressing

23) Product Images from "Adipose-derived mesenchymal stem cells formed acinar-like structure when stimulated with breast epithelial cells in three-dimensional culture"

Article Title: Adipose-derived mesenchymal stem cells formed acinar-like structure when stimulated with breast epithelial cells in three-dimensional culture

Journal: PLoS ONE

doi: 10.1371/journal.pone.0204077

Analyses of stem cell markers and angiogenic factors expression by immunofluorescence showing CM downregulated the stemness and angiogenic differentiation of ASCs in 3D. Representative fluorescence images of ASCs and HASCs stained for KRT8, stem cell markers (CD29, CD90) and angiogenic factors (CD31, VEGF). Nuclei were stained with DAPI (blue). Scale bar = 20μm.
Figure Legend Snippet: Analyses of stem cell markers and angiogenic factors expression by immunofluorescence showing CM downregulated the stemness and angiogenic differentiation of ASCs in 3D. Representative fluorescence images of ASCs and HASCs stained for KRT8, stem cell markers (CD29, CD90) and angiogenic factors (CD31, VEGF). Nuclei were stained with DAPI (blue). Scale bar = 20μm.

Techniques Used: Expressing, Immunofluorescence, Fluorescence, Staining

24) Product Images from "Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1"

Article Title: Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1

Journal: Experimental & Molecular Medicine

doi: 10.1038/s12276-018-0133-y

RT-qPCR and Western blot analysis demonstrated that MBNL1-AS1 reduced the expression of KCNMA1 and cGMP-PKG signaling pathway-related genes. a RT-qPCR measured the relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. b Protein bands measured by Western blot analysis. c Western blot analysis measured the relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily M alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, p-PKGII phosphorylated-PKGII, VASP vasodilator-stimulated phosphoprotein, p-VASP phosphorylated-VASP, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, si small interfering, GAPDH glyceraldehyde-3-phosphate dehydrogenase, NC negative control; * p
Figure Legend Snippet: RT-qPCR and Western blot analysis demonstrated that MBNL1-AS1 reduced the expression of KCNMA1 and cGMP-PKG signaling pathway-related genes. a RT-qPCR measured the relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. b Protein bands measured by Western blot analysis. c Western blot analysis measured the relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily M alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, p-PKGII phosphorylated-PKGII, VASP vasodilator-stimulated phosphoprotein, p-VASP phosphorylated-VASP, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, si small interfering, GAPDH glyceraldehyde-3-phosphate dehydrogenase, NC negative control; * p

Techniques Used: Quantitative RT-PCR, Western Blot, Expressing, Transfection, Negative Control

MBNL1-AS1 was highly expressed, but KCNMA1 and cGMP-PKG pathway-related factors were poorly expressed in mice with I/R injury after TKA. a Relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in the skeletal muscle tissues of mice detected by RT-qPCR. b Protein bands observed after Western blot analysis. c Relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle tissues of mice evaluated by Western blot analysis. I/R ischemia-reperfusion, Sevo sevoflurane, MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, VASP vasodilator-stimulated phosphoprotein, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, GAPDH glyceraldehyde-3-phosphate dehydrogenase; * p
Figure Legend Snippet: MBNL1-AS1 was highly expressed, but KCNMA1 and cGMP-PKG pathway-related factors were poorly expressed in mice with I/R injury after TKA. a Relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in the skeletal muscle tissues of mice detected by RT-qPCR. b Protein bands observed after Western blot analysis. c Relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle tissues of mice evaluated by Western blot analysis. I/R ischemia-reperfusion, Sevo sevoflurane, MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, VASP vasodilator-stimulated phosphoprotein, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, GAPDH glyceraldehyde-3-phosphate dehydrogenase; * p

Techniques Used: Mouse Assay, Expressing, Quantitative RT-PCR, Western Blot

25) Product Images from "Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway"

Article Title: Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway

Journal: Journal of Ophthalmology

doi: 10.1155/2018/5708537

Western blot analysis of protein in RPE cells. The results of the western blot analysis revealed that, VEGF, VEGFR2, and p-AKT protein expression levels were significantly downregulated in the FMOD-siRNA group, while Akt, ERK1/2 and p-ERK1/2 expression levels did not differ between the two groups: (a) representative blot images; (b) and (c): statistical analysis of western blot data. Data are represented as the means ± SEM of fold changes compared to the controls. Each experiment was repeated at least three times. ∗ P
Figure Legend Snippet: Western blot analysis of protein in RPE cells. The results of the western blot analysis revealed that, VEGF, VEGFR2, and p-AKT protein expression levels were significantly downregulated in the FMOD-siRNA group, while Akt, ERK1/2 and p-ERK1/2 expression levels did not differ between the two groups: (a) representative blot images; (b) and (c): statistical analysis of western blot data. Data are represented as the means ± SEM of fold changes compared to the controls. Each experiment was repeated at least three times. ∗ P

Techniques Used: Western Blot, Expressing

26) Product Images from "Rho GTPase Activating Protein 24 (ARHGAP24) Silencing Promotes Lung Cancer Cell Migration and Invasion by Activating β-Catenin Signaling"

Article Title: Rho GTPase Activating Protein 24 (ARHGAP24) Silencing Promotes Lung Cancer Cell Migration and Invasion by Activating β-Catenin Signaling

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.911503

ARHGAP24 overexpression inhibits MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in A549 cells. After A549 cells were subjected to blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection, the migration was assessed in in vitro would healing assay ( A ), and protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin of A549 cells was measured by Western blot analysis ( B, C ). ** P
Figure Legend Snippet: ARHGAP24 overexpression inhibits MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in A549 cells. After A549 cells were subjected to blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection, the migration was assessed in in vitro would healing assay ( A ), and protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin of A549 cells was measured by Western blot analysis ( B, C ). ** P

Techniques Used: Over Expression, Expressing, Transfection, Migration, In Vitro, Western Blot

ARHGAP24 silencing promotes MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in NCI-H1975 cells. The migration was assessed in in vitro would healing assay ( A ), and the protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin in NCI-H1975 cells with blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection in the absence or presence of 10 μM XAV-939 treatment was measured by Western blot analysis ( B, C ). ** P
Figure Legend Snippet: ARHGAP24 silencing promotes MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in NCI-H1975 cells. The migration was assessed in in vitro would healing assay ( A ), and the protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin in NCI-H1975 cells with blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection in the absence or presence of 10 μM XAV-939 treatment was measured by Western blot analysis ( B, C ). ** P

Techniques Used: Expressing, Migration, In Vitro, Transfection, Western Blot

27) Product Images from "Rho GTPase Activating Protein 24 (ARHGAP24) Silencing Promotes Lung Cancer Cell Migration and Invasion by Activating β-Catenin Signaling"

Article Title: Rho GTPase Activating Protein 24 (ARHGAP24) Silencing Promotes Lung Cancer Cell Migration and Invasion by Activating β-Catenin Signaling

Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

doi: 10.12659/MSM.911503

ARHGAP24 overexpression inhibits MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in A549 cells. After A549 cells were subjected to blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection, the migration was assessed in in vitro would healing assay ( A ), and protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin of A549 cells was measured by Western blot analysis ( B, C ). ** P
Figure Legend Snippet: ARHGAP24 overexpression inhibits MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in A549 cells. After A549 cells were subjected to blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection, the migration was assessed in in vitro would healing assay ( A ), and protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin of A549 cells was measured by Western blot analysis ( B, C ). ** P

Techniques Used: Over Expression, Expressing, Transfection, Migration, In Vitro, Western Blot

ARHGAP24 silencing promotes MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in NCI-H1975 cells. The migration was assessed in in vitro would healing assay ( A ), and the protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin in NCI-H1975 cells with blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection in the absence or presence of 10 μM XAV-939 treatment was measured by Western blot analysis ( B, C ). ** P
Figure Legend Snippet: ARHGAP24 silencing promotes MMP9, VEGF, Vimentin, E-cadherin, and β-catenin expression in NCI-H1975 cells. The migration was assessed in in vitro would healing assay ( A ), and the protein expression of MMP9, VEGF, Vimentin, E-cadherin, and β-catenin in NCI-H1975 cells with blank pLVX-Puro or pLVX-Puro-ARHGAP24 transfection in the absence or presence of 10 μM XAV-939 treatment was measured by Western blot analysis ( B, C ). ** P

Techniques Used: Expressing, Migration, In Vitro, Transfection, Western Blot

28) Product Images from "Combined effects of Lenvatinib and iodine-131 on cell apoptosis in nasopharyngeal carcinoma through inducing endoplasmic reticulum stress"

Article Title: Combined effects of Lenvatinib and iodine-131 on cell apoptosis in nasopharyngeal carcinoma through inducing endoplasmic reticulum stress

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2018.6652

In vivo effects of combined treatment of LEB and I-131 in an NPC xenograft mice model. (A) Effects of combined treatment of LEB and I-131 on tumor growth in NPC xenograft mice model. (B) Apoptotic bodies in tumors following treatment with LEB or/and I-131 determined by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay (magnification, ×20). (C) JNK and Caspase-3 expression levels in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (D) Expression levels of TNF-α and HIF-1α in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (E) Angiogenesis and VEGF expression in tumors following treatment with LEB or/and I-131 determined by hematoxylin and eosin staining (magnification, ×20). **P
Figure Legend Snippet: In vivo effects of combined treatment of LEB and I-131 in an NPC xenograft mice model. (A) Effects of combined treatment of LEB and I-131 on tumor growth in NPC xenograft mice model. (B) Apoptotic bodies in tumors following treatment with LEB or/and I-131 determined by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay (magnification, ×20). (C) JNK and Caspase-3 expression levels in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (D) Expression levels of TNF-α and HIF-1α in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (E) Angiogenesis and VEGF expression in tumors following treatment with LEB or/and I-131 determined by hematoxylin and eosin staining (magnification, ×20). **P

Techniques Used: In Vivo, Mouse Assay, End Labeling, Expressing, Immunohistochemistry, Staining

Combination of LEB and I-131 promotes apoptosis of nasopharyngeal carcinoma cells and inhibits tumor angiogenesis-related protein in vitro . (A) Apoptosis rate of HK-1 cells following treatment with LEB or/and I-131 determined by flow cytometry. (B) Protein expression levels of Caspase-3 and Caspase-9 in HK-1 cells determined by western blotting. (C) Protein expression levels of Bcl-2 and P53 in HK-1 cells determined by western blotting. (D) VEGF and PDGF expression levels in HK-1 cells determined by western blotting. The data are presented as the mean + standard error of the mean of three independent experiments. *P
Figure Legend Snippet: Combination of LEB and I-131 promotes apoptosis of nasopharyngeal carcinoma cells and inhibits tumor angiogenesis-related protein in vitro . (A) Apoptosis rate of HK-1 cells following treatment with LEB or/and I-131 determined by flow cytometry. (B) Protein expression levels of Caspase-3 and Caspase-9 in HK-1 cells determined by western blotting. (C) Protein expression levels of Bcl-2 and P53 in HK-1 cells determined by western blotting. (D) VEGF and PDGF expression levels in HK-1 cells determined by western blotting. The data are presented as the mean + standard error of the mean of three independent experiments. *P

Techniques Used: In Vitro, Flow Cytometry, Cytometry, Expressing, Western Blot

29) Product Images from "Effect of bee venom on IL-6, COX-2 and VEGF levels in polycystic ovarian syndrome induced in Wistar rats by estradiol valerate"

Article Title: Effect of bee venom on IL-6, COX-2 and VEGF levels in polycystic ovarian syndrome induced in Wistar rats by estradiol valerate

Journal: The Journal of Venomous Animals and Toxins Including Tropical Diseases

doi: 10.1186/1678-9199-19-32

Negative and positive controls for COX-2 and VEGF. Negative controls were included in each experiment by incubating tissue sections with antibody dilution buffer instead of the primary antibody (antral follicle cells). Positive control slides consisted of rat hippocampus cells for COX-2 (left panel) and vessels of corpus luteum for VEGF (right panel).
Figure Legend Snippet: Negative and positive controls for COX-2 and VEGF. Negative controls were included in each experiment by incubating tissue sections with antibody dilution buffer instead of the primary antibody (antral follicle cells). Positive control slides consisted of rat hippocampus cells for COX-2 (left panel) and vessels of corpus luteum for VEGF (right panel).

Techniques Used: Positive Control

30) Product Images from "Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney"

Article Title: Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Journal: American Journal of Physiology - Renal Physiology

doi: 10.1152/ajprenal.00523.2016

Renal VCAM-1, VEGF, and endostatin levels following VILI, CLP, or CLP+VILI. In kidney homogenates, protein levels of VCAM-1, VEGF, and endostatin were determined by Western blot analysis. All groups were run on the same gel. n = 4 mice for each group. VCAM-1 level in CLP+VILI vs. CLP ( P = 0.08). (* P
Figure Legend Snippet: Renal VCAM-1, VEGF, and endostatin levels following VILI, CLP, or CLP+VILI. In kidney homogenates, protein levels of VCAM-1, VEGF, and endostatin were determined by Western blot analysis. All groups were run on the same gel. n = 4 mice for each group. VCAM-1 level in CLP+VILI vs. CLP ( P = 0.08). (* P

Techniques Used: Western Blot, Mouse Assay

31) Product Images from "P311 Deficiency Leads to Attenuated Angiogenesis in Cutaneous Wound Healing"

Article Title: P311 Deficiency Leads to Attenuated Angiogenesis in Cutaneous Wound Healing

Journal: Frontiers in Physiology

doi: 10.3389/fphys.2017.01004

Effect of P311 expression on wound angiogenesis. (A) IHC staining of granulation tissues (day 5) for CD31, VEGF, and TGFβ1. (B) Western blot showed the expression of CD31, VEGF, and TGFβ1 in each group. Quantitation of the protein levels of CD31, VEGF, and TGFβ1 in each group (day 5). Levels of VEGF (C) and TGFβ1 (D) releasing during skin wound (day 5) were measured by sandwich ELISA. Data were expressed as means ± SD . n = 5 per group. * P
Figure Legend Snippet: Effect of P311 expression on wound angiogenesis. (A) IHC staining of granulation tissues (day 5) for CD31, VEGF, and TGFβ1. (B) Western blot showed the expression of CD31, VEGF, and TGFβ1 in each group. Quantitation of the protein levels of CD31, VEGF, and TGFβ1 in each group (day 5). Levels of VEGF (C) and TGFβ1 (D) releasing during skin wound (day 5) were measured by sandwich ELISA. Data were expressed as means ± SD . n = 5 per group. * P

Techniques Used: Expressing, Immunohistochemistry, Staining, Western Blot, Quantitation Assay, Sandwich ELISA

32) Product Images from "Neuropilin-2 promotes branching morphogenesis in the mouse mammary gland"

Article Title: Neuropilin-2 promotes branching morphogenesis in the mouse mammary gland

Journal: Development (Cambridge, England)

doi: 10.1242/dev.051318

VEGF/NRP2 signaling activates FAK, which contributes to branching morphogenesis . ( A ) Mammary glands from MMTV-Cre, MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP mice were immunostained with an antibody (Ab) specific for mouse VEGF or the appropriate control IgG. Note the intense cytoplasmic staining for VEGF in all of the glands. Scale bar: 10 μm. ( B ) Mammary glands from 5-week-old MMTV-Cre, MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP mice were immunostained with an Ab specific for p-FAK (Y397) and representative staining is shown. Immunostaining was quantified by scoring the intensity of staining of each gland on a scale of 1-5. Only scores of 4 and 5 were considered positive staining and the data are reported as the intensity of staining in the MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP glands relative to the MMTV-Cre glands. Error bars represent s.d., * P
Figure Legend Snippet: VEGF/NRP2 signaling activates FAK, which contributes to branching morphogenesis . ( A ) Mammary glands from MMTV-Cre, MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP mice were immunostained with an antibody (Ab) specific for mouse VEGF or the appropriate control IgG. Note the intense cytoplasmic staining for VEGF in all of the glands. Scale bar: 10 μm. ( B ) Mammary glands from 5-week-old MMTV-Cre, MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP mice were immunostained with an Ab specific for p-FAK (Y397) and representative staining is shown. Immunostaining was quantified by scoring the intensity of staining of each gland on a scale of 1-5. Only scores of 4 and 5 were considered positive staining and the data are reported as the intensity of staining in the MMTV-Cre;NRP2 +/loxP and MMTV-Cre;NRP2 loxP/loxP glands relative to the MMTV-Cre glands. Error bars represent s.d., * P

Techniques Used: Mouse Assay, Staining, Immunostaining

33) Product Images from "Antitumor Effects of Umbelliprenin in a Mouse Model of Colorectal Cancer"

Article Title: Antitumor Effects of Umbelliprenin in a Mouse Model of Colorectal Cancer

Journal: Iranian Journal of Pharmaceutical Research : IJPR

doi:

Photography of Immunohistochemical staining of Ki-67, CD31, VEGF, MMP2, MMP9 and E-cadherin in tumor-bearing mice
Figure Legend Snippet: Photography of Immunohistochemical staining of Ki-67, CD31, VEGF, MMP2, MMP9 and E-cadherin in tumor-bearing mice

Techniques Used: Immunohistochemistry, Staining, Mouse Assay

Immunohistochemical results of Ki-67, CD31, VEGF, MMP2, MMP9 and E-cadherin in tumor groups treated with umbelliprenin (A), liquid paraffin (B) or normal saline (C).
Figure Legend Snippet: Immunohistochemical results of Ki-67, CD31, VEGF, MMP2, MMP9 and E-cadherin in tumor groups treated with umbelliprenin (A), liquid paraffin (B) or normal saline (C).

Techniques Used: Immunohistochemistry

34) Product Images from "SARI inhibits angiogenesis and tumour growth of human colon cancer through directly targeting ceruloplasmin"

Article Title: SARI inhibits angiogenesis and tumour growth of human colon cancer through directly targeting ceruloplasmin

Journal: Nature Communications

doi: 10.1038/ncomms11996

SARI inhibits angiogenesis through inhibiting Cp expression and the activity of the HIF-1α/VEGF axis. ( a ) Immunoblots of SARI and HIF-1α expression in SW480 and HCT116 cells after stable expression of SARI. HCT116-control and HCT116-SARI cells were incubated under 1% O 2 for 48 h or treated with DMOG for 24 h. β-Actin was used as a loading control. ( b ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells with or without PX-478 (45 μM) or Tm (4.0 μM) treatment under normoxia and hypoxia. GAPDH was used as the loading control. ( c ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells after transfection with or without p-Cp plasmid under normoxia and hypoxia. GAPDH was used as the loading control. ( d ) Expression of VEGF exacted by SW480-control and SW480-SARI cells with or without Tm (4.0 μM) and PX-478 (45 μM) treatment, after transfection with or without Cp expression plasmid ( n =3; ** P
Figure Legend Snippet: SARI inhibits angiogenesis through inhibiting Cp expression and the activity of the HIF-1α/VEGF axis. ( a ) Immunoblots of SARI and HIF-1α expression in SW480 and HCT116 cells after stable expression of SARI. HCT116-control and HCT116-SARI cells were incubated under 1% O 2 for 48 h or treated with DMOG for 24 h. β-Actin was used as a loading control. ( b ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells with or without PX-478 (45 μM) or Tm (4.0 μM) treatment under normoxia and hypoxia. GAPDH was used as the loading control. ( c ) Immunoblots of Cp, HIF-1α and VEGF expression in control and SARI cells after transfection with or without p-Cp plasmid under normoxia and hypoxia. GAPDH was used as the loading control. ( d ) Expression of VEGF exacted by SW480-control and SW480-SARI cells with or without Tm (4.0 μM) and PX-478 (45 μM) treatment, after transfection with or without Cp expression plasmid ( n =3; ** P

Techniques Used: Expressing, Activity Assay, Western Blot, Incubation, Transfection, Plasmid Preparation

35) Product Images from "Combined effects of Lenvatinib and iodine-131 on cell apoptosis in nasopharyngeal carcinoma through inducing endoplasmic reticulum stress"

Article Title: Combined effects of Lenvatinib and iodine-131 on cell apoptosis in nasopharyngeal carcinoma through inducing endoplasmic reticulum stress

Journal: Experimental and Therapeutic Medicine

doi: 10.3892/etm.2018.6652

In vivo effects of combined treatment of LEB and I-131 in an NPC xenograft mice model. (A) Effects of combined treatment of LEB and I-131 on tumor growth in NPC xenograft mice model. (B) Apoptotic bodies in tumors following treatment with LEB or/and I-131 determined by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay (magnification, ×20). (C) JNK and Caspase-3 expression levels in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (D) Expression levels of TNF-α and HIF-1α in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (E) Angiogenesis and VEGF expression in tumors following treatment with LEB or/and I-131 determined by hematoxylin and eosin staining (magnification, ×20). **P
Figure Legend Snippet: In vivo effects of combined treatment of LEB and I-131 in an NPC xenograft mice model. (A) Effects of combined treatment of LEB and I-131 on tumor growth in NPC xenograft mice model. (B) Apoptotic bodies in tumors following treatment with LEB or/and I-131 determined by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay (magnification, ×20). (C) JNK and Caspase-3 expression levels in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (D) Expression levels of TNF-α and HIF-1α in tumors following treatment with LEB or/and I-131 determined by immunohistochemistry (magnification, ×20). (E) Angiogenesis and VEGF expression in tumors following treatment with LEB or/and I-131 determined by hematoxylin and eosin staining (magnification, ×20). **P

Techniques Used: In Vivo, Mouse Assay, End Labeling, Expressing, Immunohistochemistry, Staining

36) Product Images from "PDCD5 inhibits osteosarcoma cell metastasis via targeting TGF-β1/Smad signaling pathway and is associated with good prognosis"

Article Title: PDCD5 inhibits osteosarcoma cell metastasis via targeting TGF-β1/Smad signaling pathway and is associated with good prognosis

Journal: American Journal of Translational Research

doi:

PDCD5 inhibits HUVECs tube formation and downregulates the expression of VEGF of OS cells. Representative phase-contrast images of the tubes that formed (magnification × 100). PDCD5 suppressed the expression of VEGF protein.
Figure Legend Snippet: PDCD5 inhibits HUVECs tube formation and downregulates the expression of VEGF of OS cells. Representative phase-contrast images of the tubes that formed (magnification × 100). PDCD5 suppressed the expression of VEGF protein.

Techniques Used: Expressing

37) Product Images from "Amelioration of diabetic nephropathy in db/db mice treated with tibetan medicine formula Siwei Jianghuang Decoction Powder extract"

Article Title: Amelioration of diabetic nephropathy in db/db mice treated with tibetan medicine formula Siwei Jianghuang Decoction Powder extract

Journal: Scientific Reports

doi: 10.1038/s41598-018-35148-2

Effect of SWJH on renal HIF-1α/VEGF/TGF-β1 expression. ( A – U ) Immunohistochemistry of HIF-1α, VEGF and TGF-β1. Original magnification ( A – U ) at 400× magnification; ( A – C ) Quantitative analyses of immunohistochemical staining of HIF-1α, VEGF and TGF-β1. * P
Figure Legend Snippet: Effect of SWJH on renal HIF-1α/VEGF/TGF-β1 expression. ( A – U ) Immunohistochemistry of HIF-1α, VEGF and TGF-β1. Original magnification ( A – U ) at 400× magnification; ( A – C ) Quantitative analyses of immunohistochemical staining of HIF-1α, VEGF and TGF-β1. * P

Techniques Used: Expressing, Immunohistochemistry, Staining

Effect of SWJH on renal HIF-1α, VEGF and TGF-β1 expression. Real-time PCR analyses of HIF-1α, VEGF and TGF-β1 mRNA levels. * P
Figure Legend Snippet: Effect of SWJH on renal HIF-1α, VEGF and TGF-β1 expression. Real-time PCR analyses of HIF-1α, VEGF and TGF-β1 mRNA levels. * P

Techniques Used: Expressing, Real-time Polymerase Chain Reaction

Effect of SWJH on renal HIF-1α, VEGF and TGF-β1 expression. ( A – D ) Western blot analyses of HIF-1α, VEGF and TGF-β1 protein levels. ** P
Figure Legend Snippet: Effect of SWJH on renal HIF-1α, VEGF and TGF-β1 expression. ( A – D ) Western blot analyses of HIF-1α, VEGF and TGF-β1 protein levels. ** P

Techniques Used: Expressing, Western Blot

38) Product Images from "Nanoscale perfluorocarbon expediates bone fracture healing through selectively activating osteoblastic differentiation and functions"

Article Title: Nanoscale perfluorocarbon expediates bone fracture healing through selectively activating osteoblastic differentiation and functions

Journal: Journal of Nanobiotechnology

doi: 10.1186/s12951-020-00641-2

Immunofluorescent analysis of fracture zones after nano-PFC treatment for 8 weeks. a Representative immunofluorescent images of specimens with staining against MMP-9, VEGF and osteocalcin (in red). Meanwhile, nuclei are counter stained with DAPI (in blue). The scale bar is 2 cm. b Comparison of relative fluorescent intensity (n = 3). *P
Figure Legend Snippet: Immunofluorescent analysis of fracture zones after nano-PFC treatment for 8 weeks. a Representative immunofluorescent images of specimens with staining against MMP-9, VEGF and osteocalcin (in red). Meanwhile, nuclei are counter stained with DAPI (in blue). The scale bar is 2 cm. b Comparison of relative fluorescent intensity (n = 3). *P

Techniques Used: Staining

39) Product Images from "RXRα provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells"

Article Title: RXRα provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells

Journal: Cell Death & Disease

doi: 10.1038/s41419-018-0610-1

The signaling pathways underlying RXRα’s impacts on cell differentiation and carcinogenesis. a Western blot analysis of FAK, AKT, ERK, and their phospharylation in MCF-7 with RXRα overexpression. b Western blot analysis of migration markers Myl9, MMP9, and ANGPTL3 in MCF-7 cells pretreated with AKT inhibitor LY294002, ERK inhibitor PD98059, and the Rho-associated protein kinase (ROCK) inhibitor Y27632 (C3). c Western blot analysis of the expression of differentiation markers EPHB4, KDR, and eNOs in HUVECs with siRXRα knockdown or/and ERα overexpression after pre-treating with AKT inhibitor LY294002. d Scheme of signaling pathways that RXRα participates. RXRα inhibits cell proliferation, angiogenesis, and migration through interacting with VEGF, ANGPTL3, and ERα. It could trigger senescence-like tumor-suppressing mechanism by upregulating p53, p21, and p16 in stem cells. It also regulates/participates in metabolism reprogramming through phosphorylation of AKT and FAK. The multiple functions suggest that RXRα may be a key cellular component in protecting stem cells from carcinogenesis
Figure Legend Snippet: The signaling pathways underlying RXRα’s impacts on cell differentiation and carcinogenesis. a Western blot analysis of FAK, AKT, ERK, and their phospharylation in MCF-7 with RXRα overexpression. b Western blot analysis of migration markers Myl9, MMP9, and ANGPTL3 in MCF-7 cells pretreated with AKT inhibitor LY294002, ERK inhibitor PD98059, and the Rho-associated protein kinase (ROCK) inhibitor Y27632 (C3). c Western blot analysis of the expression of differentiation markers EPHB4, KDR, and eNOs in HUVECs with siRXRα knockdown or/and ERα overexpression after pre-treating with AKT inhibitor LY294002. d Scheme of signaling pathways that RXRα participates. RXRα inhibits cell proliferation, angiogenesis, and migration through interacting with VEGF, ANGPTL3, and ERα. It could trigger senescence-like tumor-suppressing mechanism by upregulating p53, p21, and p16 in stem cells. It also regulates/participates in metabolism reprogramming through phosphorylation of AKT and FAK. The multiple functions suggest that RXRα may be a key cellular component in protecting stem cells from carcinogenesis

Techniques Used: Cell Differentiation, Western Blot, Over Expression, Migration, Expressing

RXR overexpression in cancer cells inhibited proliferation, migration, and angiogenesis. a MTT assay and b EdU assay of MCF-7 transfected with RXRα after 48 h. c Flow cytometry detection of the cell cycle distribution of MCF-7 48 h after transfecting with RXRα. The migratory ability of MCF-7 overexpressing RXRα was determined via wound healing ( d ) and transwell chamber assays ( e ) as described in “Materials and methods”). The expression of Cyr61, Myl9, and MMP9 examined by qRT-PCR ( f ) and western blotting ( g ). h SA-β-galactosidase staining assay of parental and RXRα overexpression MCF-7 cells. i The expressions of ANGPTL3 and VEGF were examined by qRT-PCR ( j ) and western blotting ( k ) in MCF-7 overexpressing RXRα. Shown are the means ± SD from three independent experiments (* P
Figure Legend Snippet: RXR overexpression in cancer cells inhibited proliferation, migration, and angiogenesis. a MTT assay and b EdU assay of MCF-7 transfected with RXRα after 48 h. c Flow cytometry detection of the cell cycle distribution of MCF-7 48 h after transfecting with RXRα. The migratory ability of MCF-7 overexpressing RXRα was determined via wound healing ( d ) and transwell chamber assays ( e ) as described in “Materials and methods”). The expression of Cyr61, Myl9, and MMP9 examined by qRT-PCR ( f ) and western blotting ( g ). h SA-β-galactosidase staining assay of parental and RXRα overexpression MCF-7 cells. i The expressions of ANGPTL3 and VEGF were examined by qRT-PCR ( j ) and western blotting ( k ) in MCF-7 overexpressing RXRα. Shown are the means ± SD from three independent experiments (* P

Techniques Used: Over Expression, Migration, MTT Assay, EdU Assay, Transfection, Flow Cytometry, Cytometry, Expressing, Quantitative RT-PCR, Western Blot, Staining

40) Product Images from "Regenerative repair of Pifithrin-α in cerebral ischemia via VEGF dependent manner"

Article Title: Regenerative repair of Pifithrin-α in cerebral ischemia via VEGF dependent manner

Journal: Scientific Reports

doi: 10.1038/srep26295

Increased expression of VEGF after inhibition of p53 in vivo and vitro . ( A ) Protein abundance of VEGF 7 days post-stroke using western blot analysis of brain homogenates (MCAo group; Vehicle group; PFT-α group). β-actin served as a loading control. ( B ) Quantitative determination showed that PFT-α significantly increased the expression of VEGF in cerebral ischemic rats. ** P
Figure Legend Snippet: Increased expression of VEGF after inhibition of p53 in vivo and vitro . ( A ) Protein abundance of VEGF 7 days post-stroke using western blot analysis of brain homogenates (MCAo group; Vehicle group; PFT-α group). β-actin served as a loading control. ( B ) Quantitative determination showed that PFT-α significantly increased the expression of VEGF in cerebral ischemic rats. ** P

Techniques Used: Expressing, Inhibition, In Vivo, Western Blot

Related Articles

Concentration Assay:

Article Title: Vascular Endothelial Growth Factor Mediates Corneal Nerve Repair
Article Snippet: .. After blocking, the following concentration of antibodies was diluted in blocking solution and applied to each membrane for 90 minutes: rat anti-VEGF164 (1:1000; R & D Systems, Minneapolis, MN); rabbit anti-VEGFR1 (1:2500, ab32152; Abcam, Cambridge, MA); rabbit anti-VEGFR2 (1:500, ab42230; Abcam); and rabbit anti-NRP1 (1:200) and rabbit anti-NRP2 (1:200) (H-286 and H-300; Santa Cruz Biotechnology). .. After washing in PBS with 0.15% Tween 20, blots were incubated with infrared-tagged anti–rat or anti–rabbit donkey secondary antibodies (1:1000; Rockland, Gilbertsville, PA) in blocking solution for 1 hour.

Incubation:

Article Title: Role and regulation of growth plate vascularization during coupling with osteogenesis in tibial dyschondroplasia of chickens
Article Snippet: .. The membranes were incubated with rabbit-source antibodies to FGF2 (Abclonal Technology, #A0235, 1:1,000), FGFR1 (Abclonal Technology, #A2073, 1:1,000), VEGFA (Abcam, #ab46154, 1:1,000) and VEGFR1 (Abcam, #ab32152, 1:1,000), and then re-probed with appropriate horseradish peroxidase-conjugated secondary antibodies (Servicebio technology, #GB23303, 1:3,000). .. The membranes were then visualized by enhanced chemiluminescence (ECL Kit, Servicebio technology, #G2014) and exposed to X-ray films.

Article Title: VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
Article Snippet: .. The membranes were incubated with different antibodies, including anti-phospho (Tyr416)-Src (#2101, Cell Signaling), anti-Src (#2123, Cell Signaling), anti-phospho (Ser473)-Akt (#4060, Cell Signaling), anti-Akt (#4691, Cell Signaling), anti-phospho (Thr202/Tyr204)-Erk1/2 (#4370, Cell Signaling), anti-Erk1/2 (#4695, Cell Signaling), anti-VEGFR1 (ab32152, Abcam), anti-NP-1 (ab81321, Abcam), and anti-VEGF-B (sc-80442, Santa Cruz). .. Immunoreactivity was detected using an HRP-conjugated secondary antibody and visualized using enhanced chemiluminescence (ECL, Thermo Scientific).

Article Title: Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1
Article Snippet: .. The membrane was then blocked in 5% skimmed milk at room temperature for 1 h, washed twice with PBS, and then incubated overnight at 4 °C with diluted rabbit anti-mouse primary antibodies against KCNMA1 (1:1000, MAB8589; AmyJet Scientific Inc., Wuhan, China), PKGII (1:1000, ab145063; Abcam, Inc., Cambridge, MA, USA), VASP (1:1000, ab58555; Abcam, USA), VEGF (1:1000, ab32152; Abcam, USA), Bax (1:1000, ab32503; Abcam, USA), Bcl-2 (1:1000, ab59348; Abcam, USA), Cyclin D1 (1:1000, ab134175, Abcam, USA), Cyclin D3 (1:1000, ab28283, Abcam, USA), Cdc 42 (1:1000, ab187643, Abcam, USA), caspase-3 (1:1000, ab208161, Abcam, USA), and PARP (1:1000, ab32064, Abcam, USA). .. After being washed 3 times in Tris-buffered saline tween-20 (TBST), the membrane was incubated with HRP-labeled goat anti-rabbit IgG secondary antibodies (1:5000) for 1 h and washed 3 times with TBST (5 min each time).

Article Title: Isolation, culture and induced differentiation of rabbit mesenchymal stem cells into osteoblasts
Article Snippet: .. Subsequently, the membrane was incubated with specific antibodies overnight at 4°C, including rabbit anti-BMP-2 antibody (ab14933; 1:1,000; Abcam), rabbit anti-VEGF antibody (ab32152; 1:4,000; Abcam) and human anti-Ct II antibody (ab159157; 1:2,000; Abcam). .. Anti-GAPDH antibody (ab181602; 1:10,000; Abcam) was selected as an internal reference.

other:

Article Title: Embryonic rat vascular smooth muscle cells revisited - a model for neonatal, neointimal SMC or differentiated vascular stem cells?
Article Snippet: Primary antibodies included: SMA (monoclonal mouse anti-α-actin antibody, Sigma Cat No: A5228), SM-MHC (monoclonal mouse anti-myosin antibody, Sigma Cat No: clone hSM-V, M7786), (anti-MHC antibody [1G12], Abcam Cat No: Ab683) and (the goat polyclonal MYH11 Antibody (N-16) from Santa Cruz, Cat No: SC79079 ), CNN1 (monoclonal mouse anti-calponin antibody, Sigma Cat No: C2687), Sox10 (monoclonal rabbit anti-Sox10 antibody, Abcam Cat No: ab155279), Sox17 (monoclonal rabbit anti-Sox17 antibody, Millipore Cat No: 09-038) and S100β (monoclonal rabbit anti-S100β antibody, Millipore Cat No: 04-1054), CD44 (polyclonal rabbit anti-CD44, Abcam Cat No: Ab24504), CD29 (monoclonal rabbit anti-CD29, Millipore Cat No: 04-1109), CD146 (monoclonal rabbit anti-CD146, Millipore Cat No: 04-1147), Sca1 (rabbit polyclonal ant-Sca1, Millipore Cat No: AB4336), c-kit (polyclonal rabbit anti-c-Kit, Bioss Cat No: bs-10005R, polyclonal rabbit anti-c-Kit, Santa Cruz Cat No: sc-168) and flt-1 (monoclonal rabbit anti-Flt-1 Abcam Cat No: ab32152) and β-actin (monoclonal mouse anti-β-actin, Sigma Cat No: A5316).

Immunohistochemistry:

Article Title: Rab25 augments cancer cell invasiveness through a β1 integrin/EGFR/VEGF-A/Snail signaling axis and expression of fascin
Article Snippet: .. Immunohistochemistry was performed with primary Rab25 (ab106175, 1:200, Abcam, Cambridge, MA, USA), VEGFR-1 (ab32152, 1:250, Abcam), Snail (ab180714, 1:100, Abcam) and fascin (ab126772, 1:250, Abcam) antibodies, as described previously. .. TCGA breast and ovarian cancer gene expression data were used to calculate the correlation between FSCN1 and SNAI1 based on Pearson’s correlation co-efficient value.

Blocking Assay:

Article Title: Vascular Endothelial Growth Factor Mediates Corneal Nerve Repair
Article Snippet: .. After blocking, the following concentration of antibodies was diluted in blocking solution and applied to each membrane for 90 minutes: rat anti-VEGF164 (1:1000; R & D Systems, Minneapolis, MN); rabbit anti-VEGFR1 (1:2500, ab32152; Abcam, Cambridge, MA); rabbit anti-VEGFR2 (1:500, ab42230; Abcam); and rabbit anti-NRP1 (1:200) and rabbit anti-NRP2 (1:200) (H-286 and H-300; Santa Cruz Biotechnology). .. After washing in PBS with 0.15% Tween 20, blots were incubated with infrared-tagged anti–rat or anti–rabbit donkey secondary antibodies (1:1000; Rockland, Gilbertsville, PA) in blocking solution for 1 hour.

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    Abcam vegf r2
    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of <t>VEGF-R2</t> signal pathway and disruption of retinal endothelial cell barrier.
    Vegf R2, supplied by Abcam, used in various techniques. Bioz Stars score: 91/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam anti vegf a
    Conformer selectivity of the peptides for different oncogenic quadruplexes in MCF-7 cells. ( A ) pGL4.72[ hRlucCP ] vector having the inserts containing oncogenic promoter sequences ( c-MYC, BCL-2, KRAS and <t>VEGF-A</t> ) and upstream G-quadruplex forming elements ahead of the hRluc coding region. The promoter sequences are cloned into KpnI and HindIII restriction sites with or without the wild-type quadruplex scaffolds. hRluc, Renilla luciferase gene; hCL1 and hPEST , protein destabilizing sequences; oriC, origin of replication; AmpR, ampicillin resistance gene; SV40 (Simian virus 40 polyadenylation signal cassette), P1 and P2, promoter sequences; null, constructs having no quadruplex motif upstream the oncogene promoters; GQ, G-quadruplex forming motif. ( B ) Dual-luciferase assays. Evaluation of the promoter activity of different oncogenes (( B ) c-MYC , ( C ) BCL-2 , ( D ) KRAS and ( E ) VEGF-A ) of using the reporter plasmids with or without the wild-type quadruplex-forming sequences (Pu27-GQ, BCL-2-GQ, KRAS-GQ and VEGF-A-GQ) in MCF-7 cells. Relative promoter activity is determined by normalizing the Rluc/Fluc values to that of the cells transfected with P1-P2 promoter construct (GQ-null), having no quadruplex-forming motif. Error bars represent mean ± SE ( N = 5). Statistical differences in the luciferase activities compared to the respective GQ-null constructs of the target oncogenes used one-way ANOVA followed by Tukey–Kramer Test ( # P
    Anti Vegf A, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    vegf  (Abcam)
    99
    Abcam vegf
    RT-qPCR and Western blot analysis demonstrated that MBNL1-AS1 reduced the expression of KCNMA1 and cGMP-PKG signaling pathway-related genes. a RT-qPCR measured the relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, <t>VASP,</t> <t>VEGF,</t> Bax, and Bcl-2 in skeletal muscle cells after transfection. b Protein bands measured by Western blot analysis. c Western blot analysis measured the relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily M alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, p-PKGII phosphorylated-PKGII, VASP vasodilator-stimulated phosphoprotein, p-VASP phosphorylated-VASP, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, si small interfering, GAPDH glyceraldehyde-3-phosphate dehydrogenase, NC negative control; * p
    Vegf, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 310 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: Proposed cascade of events following activation of 12/15-LOX by hyperglycemia. Lipid metabolites of 12/15-LOX (12- and 15-HETE) activate vascular NADPH oxidase leading to overproduction of reactive oxygen species (ROS). Generation of ROS suppresses the activity of protein tyrosine phosphatases with subsequent activation of VEGF-R2 signal pathway and disruption of retinal endothelial cell barrier.

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: Activation Assay, Activity Assay

    12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: 12-HETE induces phosphorylation of VEGF-R2 and dephosphorylation of protein tyrosine phosphatase (PTP) SHP1 in REC. Western blotting analysis (A) demonstrated significant increase in the level of pVEGF-R2 after 5 and 60 minutes from the beginning of treatment with 12-HETE. *P

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: De-Phosphorylation Assay, Western Blot

    Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Journal: PLoS ONE

    Article Title: 12/15-Lipoxygenase-Derived Lipid Metabolites Induce Retinal Endothelial Cell Barrier Dysfunction: Contribution of NADPH Oxidase

    doi: 10.1371/journal.pone.0057254

    Figure Lengend Snippet: Effect of VEGF-R2 inhibition on 12-HETE-induced REC hyperpermeability. Retinal endothelial cells were treated with 0.1 µM 12-HETE in the presence or absence of the VEGF-R2 inhibitor, ZM323881 hydrochloride (10 nM) for 12 hrs before adding the FITC-dextran to the upper chamber of the transwell. Four hrs later the fluorescence intensity in the lower chamber was measured by the plate reader and corrected to the intensity in the upper one. The permeability effect of 12-HETE was significantly prevented by the ZM323881 hydrochloride (12-HETE+I). * P

    Article Snippet: In particular, NADPH oxidase has been shown to modulate VEGF signaling pathway in endothelial cells via activating VEGF-R2 , .

    Techniques: Inhibition, Fluorescence, Permeability

    Conformer selectivity of the peptides for different oncogenic quadruplexes in MCF-7 cells. ( A ) pGL4.72[ hRlucCP ] vector having the inserts containing oncogenic promoter sequences ( c-MYC, BCL-2, KRAS and VEGF-A ) and upstream G-quadruplex forming elements ahead of the hRluc coding region. The promoter sequences are cloned into KpnI and HindIII restriction sites with or without the wild-type quadruplex scaffolds. hRluc, Renilla luciferase gene; hCL1 and hPEST , protein destabilizing sequences; oriC, origin of replication; AmpR, ampicillin resistance gene; SV40 (Simian virus 40 polyadenylation signal cassette), P1 and P2, promoter sequences; null, constructs having no quadruplex motif upstream the oncogene promoters; GQ, G-quadruplex forming motif. ( B ) Dual-luciferase assays. Evaluation of the promoter activity of different oncogenes (( B ) c-MYC , ( C ) BCL-2 , ( D ) KRAS and ( E ) VEGF-A ) of using the reporter plasmids with or without the wild-type quadruplex-forming sequences (Pu27-GQ, BCL-2-GQ, KRAS-GQ and VEGF-A-GQ) in MCF-7 cells. Relative promoter activity is determined by normalizing the Rluc/Fluc values to that of the cells transfected with P1-P2 promoter construct (GQ-null), having no quadruplex-forming motif. Error bars represent mean ± SE ( N = 5). Statistical differences in the luciferase activities compared to the respective GQ-null constructs of the target oncogenes used one-way ANOVA followed by Tukey–Kramer Test ( # P

    Journal: Nucleic Acids Research

    Article Title: Site-specific amino acid substitution in dodecameric peptides determines the stability and unfolding of c-MYC quadruplex promoting apoptosis in cancer cells

    doi: 10.1093/nar/gky824

    Figure Lengend Snippet: Conformer selectivity of the peptides for different oncogenic quadruplexes in MCF-7 cells. ( A ) pGL4.72[ hRlucCP ] vector having the inserts containing oncogenic promoter sequences ( c-MYC, BCL-2, KRAS and VEGF-A ) and upstream G-quadruplex forming elements ahead of the hRluc coding region. The promoter sequences are cloned into KpnI and HindIII restriction sites with or without the wild-type quadruplex scaffolds. hRluc, Renilla luciferase gene; hCL1 and hPEST , protein destabilizing sequences; oriC, origin of replication; AmpR, ampicillin resistance gene; SV40 (Simian virus 40 polyadenylation signal cassette), P1 and P2, promoter sequences; null, constructs having no quadruplex motif upstream the oncogene promoters; GQ, G-quadruplex forming motif. ( B ) Dual-luciferase assays. Evaluation of the promoter activity of different oncogenes (( B ) c-MYC , ( C ) BCL-2 , ( D ) KRAS and ( E ) VEGF-A ) of using the reporter plasmids with or without the wild-type quadruplex-forming sequences (Pu27-GQ, BCL-2-GQ, KRAS-GQ and VEGF-A-GQ) in MCF-7 cells. Relative promoter activity is determined by normalizing the Rluc/Fluc values to that of the cells transfected with P1-P2 promoter construct (GQ-null), having no quadruplex-forming motif. Error bars represent mean ± SE ( N = 5). Statistical differences in the luciferase activities compared to the respective GQ-null constructs of the target oncogenes used one-way ANOVA followed by Tukey–Kramer Test ( # P

    Article Snippet: Santacruz Biotechnology Inc.), anti E2F1, anti VEGF-A, anti-P53, anti-APAF1, anti-Caspase 8, anti-PARP (Abcam), anti-β-actin (Mouse monoclonal, 1:10 000 dil.

    Techniques: Plasmid Preparation, Clone Assay, Luciferase, Construct, Activity Assay, Transfection

    Selective arresting of c-MYC quadruplex by KR12C induce apoptotic signalling in cancer cells. ( A ) Western blot analyses of the major apoptotic markers (BCL-2, APAF-1, caspase 8 and PARP). ( B ) Estimation of protein expression level of the apoptotic markers by semi-densitometric analyses. Estimation of BCL-2 transcripts by real time PCR analyses at 5 and 10 μM KR12C concentration. ( C ) Western blot analyses of other proteins associated with the signalling cascade (c-MYC, E2F-1, VEGF-A and P53). ( D ) Quatification of protein and mRNA expression level of c-MYC, E2F-1, VEGF-A and P53 by semi-densitometric analyses and real time PCR respectively. Arrow pointing upwards and downwards denote the upregulation of the respective protein and mRNA expression level. Error bars represent mean ± SE ( N = 3). Statistical differences are determined compared to the control by two-tailed Student's t test (* P

    Journal: Nucleic Acids Research

    Article Title: Site-specific amino acid substitution in dodecameric peptides determines the stability and unfolding of c-MYC quadruplex promoting apoptosis in cancer cells

    doi: 10.1093/nar/gky824

    Figure Lengend Snippet: Selective arresting of c-MYC quadruplex by KR12C induce apoptotic signalling in cancer cells. ( A ) Western blot analyses of the major apoptotic markers (BCL-2, APAF-1, caspase 8 and PARP). ( B ) Estimation of protein expression level of the apoptotic markers by semi-densitometric analyses. Estimation of BCL-2 transcripts by real time PCR analyses at 5 and 10 μM KR12C concentration. ( C ) Western blot analyses of other proteins associated with the signalling cascade (c-MYC, E2F-1, VEGF-A and P53). ( D ) Quatification of protein and mRNA expression level of c-MYC, E2F-1, VEGF-A and P53 by semi-densitometric analyses and real time PCR respectively. Arrow pointing upwards and downwards denote the upregulation of the respective protein and mRNA expression level. Error bars represent mean ± SE ( N = 3). Statistical differences are determined compared to the control by two-tailed Student's t test (* P

    Article Snippet: Santacruz Biotechnology Inc.), anti E2F1, anti VEGF-A, anti-P53, anti-APAF1, anti-Caspase 8, anti-PARP (Abcam), anti-β-actin (Mouse monoclonal, 1:10 000 dil.

    Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction, Concentration Assay, Two Tailed Test

    Schematic representation showing selective quadruplex interaction at c-MYC promoter by KR12C promotes apoptotic signalling in VEGF-A-BCL-2 axis in MCF-7 cells.

    Journal: Nucleic Acids Research

    Article Title: Site-specific amino acid substitution in dodecameric peptides determines the stability and unfolding of c-MYC quadruplex promoting apoptosis in cancer cells

    doi: 10.1093/nar/gky824

    Figure Lengend Snippet: Schematic representation showing selective quadruplex interaction at c-MYC promoter by KR12C promotes apoptotic signalling in VEGF-A-BCL-2 axis in MCF-7 cells.

    Article Snippet: Santacruz Biotechnology Inc.), anti E2F1, anti VEGF-A, anti-P53, anti-APAF1, anti-Caspase 8, anti-PARP (Abcam), anti-β-actin (Mouse monoclonal, 1:10 000 dil.

    Techniques:

    RT-qPCR and Western blot analysis demonstrated that MBNL1-AS1 reduced the expression of KCNMA1 and cGMP-PKG signaling pathway-related genes. a RT-qPCR measured the relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. b Protein bands measured by Western blot analysis. c Western blot analysis measured the relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily M alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, p-PKGII phosphorylated-PKGII, VASP vasodilator-stimulated phosphoprotein, p-VASP phosphorylated-VASP, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, si small interfering, GAPDH glyceraldehyde-3-phosphate dehydrogenase, NC negative control; * p

    Journal: Experimental & Molecular Medicine

    Article Title: Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1

    doi: 10.1038/s12276-018-0133-y

    Figure Lengend Snippet: RT-qPCR and Western blot analysis demonstrated that MBNL1-AS1 reduced the expression of KCNMA1 and cGMP-PKG signaling pathway-related genes. a RT-qPCR measured the relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. b Protein bands measured by Western blot analysis. c Western blot analysis measured the relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle cells after transfection. MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily M alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, p-PKGII phosphorylated-PKGII, VASP vasodilator-stimulated phosphoprotein, p-VASP phosphorylated-VASP, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, si small interfering, GAPDH glyceraldehyde-3-phosphate dehydrogenase, NC negative control; * p

    Article Snippet: The membrane was then blocked in 5% skimmed milk at room temperature for 1 h, washed twice with PBS, and then incubated overnight at 4 °C with diluted rabbit anti-mouse primary antibodies against KCNMA1 (1:1000, MAB8589; AmyJet Scientific Inc., Wuhan, China), PKGII (1:1000, ab145063; Abcam, Inc., Cambridge, MA, USA), VASP (1:1000, ab58555; Abcam, USA), VEGF (1:1000, ab32152; Abcam, USA), Bax (1:1000, ab32503; Abcam, USA), Bcl-2 (1:1000, ab59348; Abcam, USA), Cyclin D1 (1:1000, ab134175, Abcam, USA), Cyclin D3 (1:1000, ab28283, Abcam, USA), Cdc 42 (1:1000, ab187643, Abcam, USA), caspase-3 (1:1000, ab208161, Abcam, USA), and PARP (1:1000, ab32064, Abcam, USA).

    Techniques: Quantitative RT-PCR, Western Blot, Expressing, Transfection, Negative Control

    MBNL1-AS1 was highly expressed, but KCNMA1 and cGMP-PKG pathway-related factors were poorly expressed in mice with I/R injury after TKA. a Relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in the skeletal muscle tissues of mice detected by RT-qPCR. b Protein bands observed after Western blot analysis. c Relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle tissues of mice evaluated by Western blot analysis. I/R ischemia-reperfusion, Sevo sevoflurane, MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, VASP vasodilator-stimulated phosphoprotein, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, GAPDH glyceraldehyde-3-phosphate dehydrogenase; * p

    Journal: Experimental & Molecular Medicine

    Article Title: Downregulation of the long noncoding RNA MBNL1-AS1 protects sevoflurane-pretreated mice against ischemia-reperfusion injury by targeting KCNMA1

    doi: 10.1038/s12276-018-0133-y

    Figure Lengend Snippet: MBNL1-AS1 was highly expressed, but KCNMA1 and cGMP-PKG pathway-related factors were poorly expressed in mice with I/R injury after TKA. a Relative mRNA expression of MBNL1-AS1, KCNMA1, PKGII, VASP, VEGF, Bax, and Bcl-2 in the skeletal muscle tissues of mice detected by RT-qPCR. b Protein bands observed after Western blot analysis. c Relative protein levels of KCNMA1, PKGII, VASP, p-PKGII, p-VASP, VEGF, Bax, and Bcl-2 in skeletal muscle tissues of mice evaluated by Western blot analysis. I/R ischemia-reperfusion, Sevo sevoflurane, MBNL1-AS1 muscleblind-like 1 antisense RNA 1, KCNMA1 potassium calcium-activated channel subfamily alpha 1, PKGII type II cyclic guanosine monophosphate-dependent protein kinase G, VASP vasodilator-stimulated phosphoprotein, VEGF vascular endothelial growth factor, Bcl-2 B-cell lymphoma/leukemia-2, Bax Bcl-2 associated X protein, GAPDH glyceraldehyde-3-phosphate dehydrogenase; * p

    Article Snippet: The membrane was then blocked in 5% skimmed milk at room temperature for 1 h, washed twice with PBS, and then incubated overnight at 4 °C with diluted rabbit anti-mouse primary antibodies against KCNMA1 (1:1000, MAB8589; AmyJet Scientific Inc., Wuhan, China), PKGII (1:1000, ab145063; Abcam, Inc., Cambridge, MA, USA), VASP (1:1000, ab58555; Abcam, USA), VEGF (1:1000, ab32152; Abcam, USA), Bax (1:1000, ab32503; Abcam, USA), Bcl-2 (1:1000, ab59348; Abcam, USA), Cyclin D1 (1:1000, ab134175, Abcam, USA), Cyclin D3 (1:1000, ab28283, Abcam, USA), Cdc 42 (1:1000, ab187643, Abcam, USA), caspase-3 (1:1000, ab208161, Abcam, USA), and PARP (1:1000, ab32064, Abcam, USA).

    Techniques: Mouse Assay, Expressing, Quantitative RT-PCR, Western Blot

    VEGF-A and VEGFR-1 are important for Snail expression. ( a ) Cells were transfected with indicated vectors. Quantitative RT-PCR (mean±s.d. * P

    Journal: Experimental & Molecular Medicine

    Article Title: Rab25 augments cancer cell invasiveness through a β1 integrin/EGFR/VEGF-A/Snail signaling axis and expression of fascin

    doi: 10.1038/emm.2017.248

    Figure Lengend Snippet: VEGF-A and VEGFR-1 are important for Snail expression. ( a ) Cells were transfected with indicated vectors. Quantitative RT-PCR (mean±s.d. * P

    Article Snippet: Immunohistochemistry was performed with primary Rab25 (ab106175, 1:200, Abcam, Cambridge, MA, USA), VEGFR-1 (ab32152, 1:250, Abcam), Snail (ab180714, 1:100, Abcam) and fascin (ab126772, 1:250, Abcam) antibodies, as described previously.

    Techniques: Expressing, Transfection, Quantitative RT-PCR