e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc e cadherin
    (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in <t>E-cadherin,</t> N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.
    E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    e cadherin - by Bioz Stars, 2023-03
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    Images

    1) Product Images from "STX5 Inhibits Hepatocellular Carcinoma Adhesion and Promotes Metastasis by Regulating the PI3K/mTOR Pathway"

    Article Title: STX5 Inhibits Hepatocellular Carcinoma Adhesion and Promotes Metastasis by Regulating the PI3K/mTOR Pathway

    Journal: Journal of Clinical and Translational Hepatology

    doi: 10.14218/JCTH.2022.00276

    (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in E-cadherin, N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.
    Figure Legend Snippet: (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in E-cadherin, N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.

    Techniques Used: Expressing, Western Blot, Transduction, Negative Control, Plasmid Preparation, Colony Assay, Transfection, Migration, Real-time Polymerase Chain Reaction

    Nude mice ( n =5) were injected with 2 × 10 6 LV-shNC or LV-shSTX5 Huh7 cells suspended in 200 µL of PBS via the tail vein. (A) Representative images of hepatic tissues from nude mice. (B) Representative images of lung tissues from nude mice. (C) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in lung tissue. (D) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in liver tissue. AFP, alpha-fetoprotein; IHC, immunohistochemical.
    Figure Legend Snippet: Nude mice ( n =5) were injected with 2 × 10 6 LV-shNC or LV-shSTX5 Huh7 cells suspended in 200 µL of PBS via the tail vein. (A) Representative images of hepatic tissues from nude mice. (B) Representative images of lung tissues from nude mice. (C) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in lung tissue. (D) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in liver tissue. AFP, alpha-fetoprotein; IHC, immunohistochemical.

    Techniques Used: Injection, Immunohistochemistry, Immunohistochemical staining

    anti e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti e cadherin
    Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and <t>E-cadherin</t> or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.
    Anti E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer"

    Article Title: Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer

    Journal: The Journal of Cell Biology

    doi: 10.1083/jcb.202203036

    Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and E-cadherin or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.
    Figure Legend Snippet: Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and E-cadherin or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.

    Techniques Used: Expressing, Staining, Two Tailed Test, MANN-WHITNEY

    Prdm16 inactivation in KSC mice resulted in acceleration of PDAC. (A) FFPE pancreatic sections from 4-mo-old control, KC, KPrC, KSC, and KSPrC mice ( n = 13–45) were stained with H&E or Alcian blue or immunostained with antibodies to CK19 or Muc5AC and subjected to IHC. Relative abundance of IPMN lesions (top left) or intensity of CK19 (top right), Muc5AC (bottom left), or Alcian blue (bottom right) are shown. Data are expressed as mean ± SEM, and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test. (B) FFPE pancreatic sections from control, KPrC, KSC, and KSPrC mice ( n = 13–45) were subjected to IF using antibodies to E-cadherin or vimentin. Representative pictures are shown. Scale bars: 50 μm. (C) Pictures of tumors harvested from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA ( n = 3). (D) FFPE liver and lung sections from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA were stained with H&E ( n = 3). Representative pictures are shown. Scale bars: 50 μm. (E) Representative pictures of soft-agar colonies formed by isogenic PANC-1 cell lines stably expressing control or PRDM16 gRNA. BxPC-3 stably expressing control or PRDM16 gRNA did not form colonies. (F) Cell proliferation assay of isogenic PANC-1 (day 3) and BxPC-3 (day 6) cell lines stably expressing control or PRDM16 gRNA. The fold increase in cell number at the end of the experiment relative to the seeding density is shown ( n = 3). Data are expressed as mean ± SEM and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test.
    Figure Legend Snippet: Prdm16 inactivation in KSC mice resulted in acceleration of PDAC. (A) FFPE pancreatic sections from 4-mo-old control, KC, KPrC, KSC, and KSPrC mice ( n = 13–45) were stained with H&E or Alcian blue or immunostained with antibodies to CK19 or Muc5AC and subjected to IHC. Relative abundance of IPMN lesions (top left) or intensity of CK19 (top right), Muc5AC (bottom left), or Alcian blue (bottom right) are shown. Data are expressed as mean ± SEM, and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test. (B) FFPE pancreatic sections from control, KPrC, KSC, and KSPrC mice ( n = 13–45) were subjected to IF using antibodies to E-cadherin or vimentin. Representative pictures are shown. Scale bars: 50 μm. (C) Pictures of tumors harvested from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA ( n = 3). (D) FFPE liver and lung sections from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA were stained with H&E ( n = 3). Representative pictures are shown. Scale bars: 50 μm. (E) Representative pictures of soft-agar colonies formed by isogenic PANC-1 cell lines stably expressing control or PRDM16 gRNA. BxPC-3 stably expressing control or PRDM16 gRNA did not form colonies. (F) Cell proliferation assay of isogenic PANC-1 (day 3) and BxPC-3 (day 6) cell lines stably expressing control or PRDM16 gRNA. The fold increase in cell number at the end of the experiment relative to the seeding density is shown ( n = 3). Data are expressed as mean ± SEM and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test.

    Techniques Used: Staining, Two Tailed Test, MANN-WHITNEY, Injection, Stable Transfection, Expressing, Proliferation Assay

    e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc e cadherin
    Effects <t>of</t> <t>ADAM12</t> on the EMT process in human colorectal cancer cells. (A) Cell adhesion was measured after AV construct or AS transfection using two cell adhesion substrates, fibronectin and collagen I. The adherent cells underwent the WST-1 assay and adhesion was quantified by measuring the absorbance at 450 nm using a plate reader. (B) Representative western blot images and semi-quantification graphs of EMT-associated proteins including MMP2, MMP9, <t>E-cadherin,</t> Snail, vimentin and claudin-1 in AV-transfected or AS-transfected DLD1 or SW480 cells. (C) Representative western blot images and semi-quantification graphs of basement membrane proteins, including integrin α5, integrin β1 and integrin β3 in AV-transfected or AS-transfected DLD1 or SW480 cells. Data are presented as the mean ± SD (n=3). * P<0.05. ADAM12, a disintegrin and metalloprotease 12; EMT, epithelial-mesenchymal transition; EV, empty pcDNA6-myc vector; AV, ADAM12-pcDNA6-myc construct; SS, scrambled siRNA; AS, ADAM12 siRNA; siRNA, small interfering RNA; MMP, matrix metalloproteinase.
    E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    e cadherin - by Bioz Stars, 2023-03
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    Images

    1) Product Images from "A disintegrin and metalloprotease 12 contributes to colorectal cancer metastasis by regulating epithelial-mesenchymal transition"

    Article Title: A disintegrin and metalloprotease 12 contributes to colorectal cancer metastasis by regulating epithelial-mesenchymal transition

    Journal: International Journal of Oncology

    doi: 10.3892/ijo.2023.5498

    Effects of ADAM12 on the EMT process in human colorectal cancer cells. (A) Cell adhesion was measured after AV construct or AS transfection using two cell adhesion substrates, fibronectin and collagen I. The adherent cells underwent the WST-1 assay and adhesion was quantified by measuring the absorbance at 450 nm using a plate reader. (B) Representative western blot images and semi-quantification graphs of EMT-associated proteins including MMP2, MMP9, E-cadherin, Snail, vimentin and claudin-1 in AV-transfected or AS-transfected DLD1 or SW480 cells. (C) Representative western blot images and semi-quantification graphs of basement membrane proteins, including integrin α5, integrin β1 and integrin β3 in AV-transfected or AS-transfected DLD1 or SW480 cells. Data are presented as the mean ± SD (n=3). * P<0.05. ADAM12, a disintegrin and metalloprotease 12; EMT, epithelial-mesenchymal transition; EV, empty pcDNA6-myc vector; AV, ADAM12-pcDNA6-myc construct; SS, scrambled siRNA; AS, ADAM12 siRNA; siRNA, small interfering RNA; MMP, matrix metalloproteinase.
    Figure Legend Snippet: Effects of ADAM12 on the EMT process in human colorectal cancer cells. (A) Cell adhesion was measured after AV construct or AS transfection using two cell adhesion substrates, fibronectin and collagen I. The adherent cells underwent the WST-1 assay and adhesion was quantified by measuring the absorbance at 450 nm using a plate reader. (B) Representative western blot images and semi-quantification graphs of EMT-associated proteins including MMP2, MMP9, E-cadherin, Snail, vimentin and claudin-1 in AV-transfected or AS-transfected DLD1 or SW480 cells. (C) Representative western blot images and semi-quantification graphs of basement membrane proteins, including integrin α5, integrin β1 and integrin β3 in AV-transfected or AS-transfected DLD1 or SW480 cells. Data are presented as the mean ± SD (n=3). * P<0.05. ADAM12, a disintegrin and metalloprotease 12; EMT, epithelial-mesenchymal transition; EV, empty pcDNA6-myc vector; AV, ADAM12-pcDNA6-myc construct; SS, scrambled siRNA; AS, ADAM12 siRNA; siRNA, small interfering RNA; MMP, matrix metalloproteinase.

    Techniques Used: Construct, Transfection, WST-1 Assay, Western Blot, Plasmid Preparation, Small Interfering RNA

    Expression of ADAM12 and E-cadherin in human CRC and lymph node tissues. Immunohistochemistry of human CRC tissues, paired N, ML or NL from the same patients stained for ADAM12 and E-cadherin. (A) Representative images of ADAM12 expression (×200 magnification) in N and CRC tissues. ADAM12 was predominantly expressed in the cytoplasm of CRC cells. (B) Representative images of E-cadherin expression (×200 magnification) in N and CRC tissues. T-WD CRC shows preserved E-cadherin expression and T-PD CRC shows decreased E-cadherin expression. (C) Representative images of ADAM12 expression (×200 magnification) ML. ADAM12 expression in ML was significantly stronger than that in NL. * P<0.05. ADAM12, a disintegrin and metalloprotease 12; CRC, colorectal cancer; N, normal colorectal mucosa; T-WD, well-differentiated tumor; T-PD, poorly differentiated tumor; NL, non-metastatic lymph node tissue; ML, metastatic lymph node tissue.
    Figure Legend Snippet: Expression of ADAM12 and E-cadherin in human CRC and lymph node tissues. Immunohistochemistry of human CRC tissues, paired N, ML or NL from the same patients stained for ADAM12 and E-cadherin. (A) Representative images of ADAM12 expression (×200 magnification) in N and CRC tissues. ADAM12 was predominantly expressed in the cytoplasm of CRC cells. (B) Representative images of E-cadherin expression (×200 magnification) in N and CRC tissues. T-WD CRC shows preserved E-cadherin expression and T-PD CRC shows decreased E-cadherin expression. (C) Representative images of ADAM12 expression (×200 magnification) ML. ADAM12 expression in ML was significantly stronger than that in NL. * P<0.05. ADAM12, a disintegrin and metalloprotease 12; CRC, colorectal cancer; N, normal colorectal mucosa; T-WD, well-differentiated tumor; T-PD, poorly differentiated tumor; NL, non-metastatic lymph node tissue; ML, metastatic lymph node tissue.

    Techniques Used: Expressing, Immunohistochemistry, Staining

    Association between ADAM12 or E-cadherin expression and the clinicopathological parameters of patients with colorectal cancer.
    Figure Legend Snippet: Association between ADAM12 or E-cadherin expression and the clinicopathological parameters of patients with colorectal cancer.

    Techniques Used: Expressing

    Kaplan-Meier survival curves of patients with CRC. Kaplan-Meier survival curves showing the association between overall survival and positive or negative expression of (A) ADAM12, (B) E-cadherin and (C) both proteins. ADAM12, a disintegrin and metalloprotease 12.
    Figure Legend Snippet: Kaplan-Meier survival curves of patients with CRC. Kaplan-Meier survival curves showing the association between overall survival and positive or negative expression of (A) ADAM12, (B) E-cadherin and (C) both proteins. ADAM12, a disintegrin and metalloprotease 12.

    Techniques Used: Expressing

    Association between ADAM12 and E-cadherin expression in human colorectal cancer.
    Figure Legend Snippet: Association between ADAM12 and E-cadherin expression in human colorectal cancer.

    Techniques Used: Expressing

    Association between survival and ADAM12 or E-cadherin expression in human colorectal cancer.
    Figure Legend Snippet: Association between survival and ADAM12 or E-cadherin expression in human colorectal cancer.

    Techniques Used: Expressing

    Effects of ADAM12 on the epithelial-mesenchymal transition process in a mouse model of peritoneal metastasis. The same number of EV AV construct-, Ssh- or Ash-transfected SW480 cells were injected intraperitoneally into non-obese diabetic/severe combined immunodeficiency mice (n=6/group). The mice injected with the AV-transfected cells showed a significant increase in ADAM12 expression and a decrease in E-cadherin expression compared with in the mice injected with the EV-transfected cells. In addition, the mice injected with the Ash-transfected cells had a significant decrease in ADAM12 expression and an increase in E-cadherin expression compared with in the mice injected with the Ssh-transfected cells. Data are presented as the mean ± SD (n=3). * P<0.05. ADAM12, a disintegrin and metalloprotease 12; EV, empty pcDNA6-myc vector; AV, ADAM12-pcDNA6-myc construct; Ssh, Scrambled pGFP-C-shLenti vector; Ash, ADAM12-pGFP-C-shLenti construct.
    Figure Legend Snippet: Effects of ADAM12 on the epithelial-mesenchymal transition process in a mouse model of peritoneal metastasis. The same number of EV AV construct-, Ssh- or Ash-transfected SW480 cells were injected intraperitoneally into non-obese diabetic/severe combined immunodeficiency mice (n=6/group). The mice injected with the AV-transfected cells showed a significant increase in ADAM12 expression and a decrease in E-cadherin expression compared with in the mice injected with the EV-transfected cells. In addition, the mice injected with the Ash-transfected cells had a significant decrease in ADAM12 expression and an increase in E-cadherin expression compared with in the mice injected with the Ssh-transfected cells. Data are presented as the mean ± SD (n=3). * P<0.05. ADAM12, a disintegrin and metalloprotease 12; EV, empty pcDNA6-myc vector; AV, ADAM12-pcDNA6-myc construct; Ssh, Scrambled pGFP-C-shLenti vector; Ash, ADAM12-pGFP-C-shLenti construct.

    Techniques Used: Construct, Transfection, Injection, Expressing, Plasmid Preparation

    anti e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti e cadherin
    A. Representative images for immunostainings of cytokeratin 8 (CK8) and α-smooth muscle actin (α-SMA) in a continuous series of placental sections. Stars indicated the invasion distance of trophoblast (CK8 positive cells) in maternal decidua (α-SMA labeled zone). B. Relative invasion area of trophoblast into decidua was quantified. C. Protein expression level of <t>E-cadherin</t> was detected in placental tissues.
    Anti E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "COMT inhibitor tolcapone represses the migration and invasion of trophoblast and results in preeclampsia-like phenotypes in mice"

    Article Title: COMT inhibitor tolcapone represses the migration and invasion of trophoblast and results in preeclampsia-like phenotypes in mice

    Journal: bioRxiv

    doi: 10.1101/2023.03.17.530517

    A. Representative images for immunostainings of cytokeratin 8 (CK8) and α-smooth muscle actin (α-SMA) in a continuous series of placental sections. Stars indicated the invasion distance of trophoblast (CK8 positive cells) in maternal decidua (α-SMA labeled zone). B. Relative invasion area of trophoblast into decidua was quantified. C. Protein expression level of E-cadherin was detected in placental tissues.
    Figure Legend Snippet: A. Representative images for immunostainings of cytokeratin 8 (CK8) and α-smooth muscle actin (α-SMA) in a continuous series of placental sections. Stars indicated the invasion distance of trophoblast (CK8 positive cells) in maternal decidua (α-SMA labeled zone). B. Relative invasion area of trophoblast into decidua was quantified. C. Protein expression level of E-cadherin was detected in placental tissues.

    Techniques Used: Labeling, Expressing

    A. Cell viability assay. HTR8/SVneo cells were treated with various dose of tolcapone for 48 h. Cell viability was measured by CCK8 assay. B. Wound healing assay of HTR8/SVneo cells treated with 25mM or 35mM tolcapone for 48 h. C. Quantification of relative healing wound width is shown. D. Measurement of cell migration by transwell assay. HTR8/SVneo cells were treated with 25mM or 35mM tolcapone for 24 h. E. Measurement of cell invasion by transwell assay. HTR8/SVneo cells treated with 25mM or 35mM tolcapone for 24 h. F. Protein expression levels of E-cadherin, Snail and Twist were detected in cells treated with 35mM tolcapone.
    Figure Legend Snippet: A. Cell viability assay. HTR8/SVneo cells were treated with various dose of tolcapone for 48 h. Cell viability was measured by CCK8 assay. B. Wound healing assay of HTR8/SVneo cells treated with 25mM or 35mM tolcapone for 48 h. C. Quantification of relative healing wound width is shown. D. Measurement of cell migration by transwell assay. HTR8/SVneo cells were treated with 25mM or 35mM tolcapone for 24 h. E. Measurement of cell invasion by transwell assay. HTR8/SVneo cells treated with 25mM or 35mM tolcapone for 24 h. F. Protein expression levels of E-cadherin, Snail and Twist were detected in cells treated with 35mM tolcapone.

    Techniques Used: Viability Assay, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Expressing

    e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc e cadherin
    E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    e cadherin  (Cell Signaling Technology Inc)


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    antibodies against e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against e cadherin
    (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of <t>E-cadherin</t> (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.
    Antibodies Against E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "High prevalence and dependence of centrosome clustering in mesenchymal tumors and leukemia"

    Article Title: High prevalence and dependence of centrosome clustering in mesenchymal tumors and leukemia

    Journal: bioRxiv

    doi: 10.1101/2023.03.13.532472

    (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.
    Figure Legend Snippet: (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.

    Techniques Used: Expressing, Western Blot, Derivative Assay

    (A) GSEA of centriole-associated gene sets with genes ranked by their association with CC in the linear model. GSEA peak enrichment scores (ES) and false discovery rates (FDR) are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (B) Volcano plots of differential gene expression associated with CC. Genes that belong to the gene sets in (A) are highlighted according to whether they are negatively (blue) or positively (red) associated with CC. (C) Barplot showing GSEA enrichment scores for all gene sets comprising mesenchymal or epithelial genes. The FDR was calculated using the full set of gene sets used in this study. Gene sets with significant genes over or under-expressed in association with CC (FDR < 0.05) are represented in red and blue, respectively. (D) T-statistic for association of protein expression with CC, linearly modelled according to the equation at the top using three independent datasets ( Gholami et al , 2013 ; Nishizuka et al , 2003 ; Guo et al , 2019 ) shows consistent, albeit not significant, negative association of E-cadherin (CDH1), β-catenin (CTNNB1) and PDLIM1 levels with CC (Table 1). PDLIM1 downregulation has been associated with metastatic potential in colorectal cancer through destabilization of the E-cadherin/β-catenin complex ( Chen et al , 2016 )
    Figure Legend Snippet: (A) GSEA of centriole-associated gene sets with genes ranked by their association with CC in the linear model. GSEA peak enrichment scores (ES) and false discovery rates (FDR) are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (B) Volcano plots of differential gene expression associated with CC. Genes that belong to the gene sets in (A) are highlighted according to whether they are negatively (blue) or positively (red) associated with CC. (C) Barplot showing GSEA enrichment scores for all gene sets comprising mesenchymal or epithelial genes. The FDR was calculated using the full set of gene sets used in this study. Gene sets with significant genes over or under-expressed in association with CC (FDR < 0.05) are represented in red and blue, respectively. (D) T-statistic for association of protein expression with CC, linearly modelled according to the equation at the top using three independent datasets ( Gholami et al , 2013 ; Nishizuka et al , 2003 ; Guo et al , 2019 ) shows consistent, albeit not significant, negative association of E-cadherin (CDH1), β-catenin (CTNNB1) and PDLIM1 levels with CC (Table 1). PDLIM1 downregulation has been associated with metastatic potential in colorectal cancer through destabilization of the E-cadherin/β-catenin complex ( Chen et al , 2016 )

    Techniques Used: Expressing

    anti e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti e cadherin
    A Western blot analysis of the expression of Rab32 after U87 and U251cells were infected with LV-Rab32 shRNA. β-Actin was used as a loading control. B Gene expression profiling was performed in Rab32 knockdown U87 cells. Enrichment analysis of differentially expressed genes (DEGs) was presented as a volcano plot; genes with more than twofold significant changes were selected. C GO analyses were conducted to predict the potential molecular functions of Rab32. The size of the dots represents the number of genes enriched in each analysis. D A wound-healing assay was employed to analyze the migratory ability of Rab32-silenced U87 and U251 cells. Scale bar = 200 μm. E The invasive capacity of Rab32-silenced U87 and U251 cells was analyzed using a transwell invasion assay. Representative images of cells crossing the membrane are shown. Scale bar = 100 μm. F Western blotting analysis was performed to detect the MMP2, MMP9, Vimentin, <t>N-cadherin,</t> and E-cadherin expression levels. β-Actin was used as a loading control. The data are shown as the mean ± SD of three replicates. *** P < 0.001 vs. NC groups.
    Anti E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission"

    Article Title: Rab32 promotes glioblastoma migration and invasion via regulation of ERK/Drp1-mediated mitochondrial fission

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-023-05721-3

    A Western blot analysis of the expression of Rab32 after U87 and U251cells were infected with LV-Rab32 shRNA. β-Actin was used as a loading control. B Gene expression profiling was performed in Rab32 knockdown U87 cells. Enrichment analysis of differentially expressed genes (DEGs) was presented as a volcano plot; genes with more than twofold significant changes were selected. C GO analyses were conducted to predict the potential molecular functions of Rab32. The size of the dots represents the number of genes enriched in each analysis. D A wound-healing assay was employed to analyze the migratory ability of Rab32-silenced U87 and U251 cells. Scale bar = 200 μm. E The invasive capacity of Rab32-silenced U87 and U251 cells was analyzed using a transwell invasion assay. Representative images of cells crossing the membrane are shown. Scale bar = 100 μm. F Western blotting analysis was performed to detect the MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin expression levels. β-Actin was used as a loading control. The data are shown as the mean ± SD of three replicates. *** P < 0.001 vs. NC groups.
    Figure Legend Snippet: A Western blot analysis of the expression of Rab32 after U87 and U251cells were infected with LV-Rab32 shRNA. β-Actin was used as a loading control. B Gene expression profiling was performed in Rab32 knockdown U87 cells. Enrichment analysis of differentially expressed genes (DEGs) was presented as a volcano plot; genes with more than twofold significant changes were selected. C GO analyses were conducted to predict the potential molecular functions of Rab32. The size of the dots represents the number of genes enriched in each analysis. D A wound-healing assay was employed to analyze the migratory ability of Rab32-silenced U87 and U251 cells. Scale bar = 200 μm. E The invasive capacity of Rab32-silenced U87 and U251 cells was analyzed using a transwell invasion assay. Representative images of cells crossing the membrane are shown. Scale bar = 100 μm. F Western blotting analysis was performed to detect the MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin expression levels. β-Actin was used as a loading control. The data are shown as the mean ± SD of three replicates. *** P < 0.001 vs. NC groups.

    Techniques Used: Western Blot, Expressing, Infection, shRNA, Wound Healing Assay, Transwell Invasion Assay

    The U87 and U251 were transfected with OE-Rab32 plasmid and then treated with 50 μM Mdivi-1 for 24 h. A Representative immunofluorescence images of the mitochondrial network (upper panel) in treaded U87 and U251 cells. Red: Tom20, Bule: DAPI. Areas in the white squares are amplified and shown in the middle. The length of mitochondria was quantified by Image J (lower panel). Scale bar = 10 μm. N = 30 per group. Data shown are mean ± SD. B TEM photomicrographs of U87MG cells with Rab32 knockdown or overexpression (upper panel). Quantification of mitochondrial length, perimeter and area using ImageJ software (lower panel). Mitochondria are highlighted in red arrows. N = 30 per group. Data shown are mean ± SD. C The migratory ability of cells was analyzed using a wound-healing assay. Scale bar = 200 μm. D A transwell invasion assay evaluated the invasive capacity of cells. Representative images of cells crossing the membrane are shown. Scale bar = 100 μm. E , F Quantitative analysis of glioma cells’ migratory and invasive capacity in C and D , respectively. G Western blotting analysis was performed to detect the level of MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin. β-Actin was used as a loading control. The data are shown as the mean ± SD of three replicates. ** P < 0.01, *** P < 0.001 vs. NC groups.
    Figure Legend Snippet: The U87 and U251 were transfected with OE-Rab32 plasmid and then treated with 50 μM Mdivi-1 for 24 h. A Representative immunofluorescence images of the mitochondrial network (upper panel) in treaded U87 and U251 cells. Red: Tom20, Bule: DAPI. Areas in the white squares are amplified and shown in the middle. The length of mitochondria was quantified by Image J (lower panel). Scale bar = 10 μm. N = 30 per group. Data shown are mean ± SD. B TEM photomicrographs of U87MG cells with Rab32 knockdown or overexpression (upper panel). Quantification of mitochondrial length, perimeter and area using ImageJ software (lower panel). Mitochondria are highlighted in red arrows. N = 30 per group. Data shown are mean ± SD. C The migratory ability of cells was analyzed using a wound-healing assay. Scale bar = 200 μm. D A transwell invasion assay evaluated the invasive capacity of cells. Representative images of cells crossing the membrane are shown. Scale bar = 100 μm. E , F Quantitative analysis of glioma cells’ migratory and invasive capacity in C and D , respectively. G Western blotting analysis was performed to detect the level of MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin. β-Actin was used as a loading control. The data are shown as the mean ± SD of three replicates. ** P < 0.01, *** P < 0.001 vs. NC groups.

    Techniques Used: Transfection, Plasmid Preparation, Immunofluorescence, Amplification, Over Expression, Software, Wound Healing Assay, Transwell Invasion Assay, Western Blot

    A Wound-healing assay was employed to analyze the migratory ability after OE Rab32- U87 and U251 cells stimulated with 1 μM SCH772984 for 24 h. Scale bar = 200 μm. B Quantitative analysis of the migratory capacity of glioma cells in A . C Transwell matrigel invasion assay was used to evaluate the invasive capacity of OE Rab32- U87 and U251 cells presence SCH772984 treatment. Scale bar = 100 μm. D Quantitative analysis of the invasion capacity of glioma cells in C . E Western blot analyzed the expression of MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin after OE Rab32- U87 and U251 cells treated with 1 μM SCH772984 for 24 h. β-Actin was used as a loading control. Data are shown as the mean ± SD of three replicates; ** P < 0.01, *** P < 0.001 vs. indicated groups.
    Figure Legend Snippet: A Wound-healing assay was employed to analyze the migratory ability after OE Rab32- U87 and U251 cells stimulated with 1 μM SCH772984 for 24 h. Scale bar = 200 μm. B Quantitative analysis of the migratory capacity of glioma cells in A . C Transwell matrigel invasion assay was used to evaluate the invasive capacity of OE Rab32- U87 and U251 cells presence SCH772984 treatment. Scale bar = 100 μm. D Quantitative analysis of the invasion capacity of glioma cells in C . E Western blot analyzed the expression of MMP2, MMP9, Vimentin, N-cadherin, and E-cadherin after OE Rab32- U87 and U251 cells treated with 1 μM SCH772984 for 24 h. β-Actin was used as a loading control. Data are shown as the mean ± SD of three replicates; ** P < 0.01, *** P < 0.001 vs. indicated groups.

    Techniques Used: Wound Healing Assay, Invasion Assay, Western Blot, Expressing

    A Representative images of tumors dissected from each group of mice were taken after nude mice were sacrificed. B The tumor volumes were measured and monitored every 5 days from each group of mice. NC or Rab32 silencing- U87 cells were subcutaneously injected into the flank of male BALB/c nude mice ( n = 5 per group). C The weights of subcutaneous NC or Rab32 silencing- U87 cells tumors on the 35th day after injection. D Kaplan–Meier survival curve of intracranial in situ xenograft tumor nude mouse model with LV-shNC or LV-shRab32 transfected U87 cells ( n = 6 per group). E Representative images of IHC staining of paraffin sections of in situ transplanted tumors in mice for Rab32, MMP2, MMP9, Vimentin N-cadherin, and E-cadherin. Scale bars = 100 μm. F Western blot analysis of Rab32, MMP2, MMP9, N-cadherin, E-cadherin, and Vimentin in situ xenograft tumors derived from NC- or Rab32 silenced -U87 cells. G Western blot analysis of Rab32, p-ERK 1/2 , ERK 1/2, p-Drp1 S616 , p-Drp1 S637 and Drp1 in xenograft tumors derived from NC- or Rab32 silenced -U87 cells. β-Actin was used as loading control. All data are shown as the mean ± SD of three replicates. ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: A Representative images of tumors dissected from each group of mice were taken after nude mice were sacrificed. B The tumor volumes were measured and monitored every 5 days from each group of mice. NC or Rab32 silencing- U87 cells were subcutaneously injected into the flank of male BALB/c nude mice ( n = 5 per group). C The weights of subcutaneous NC or Rab32 silencing- U87 cells tumors on the 35th day after injection. D Kaplan–Meier survival curve of intracranial in situ xenograft tumor nude mouse model with LV-shNC or LV-shRab32 transfected U87 cells ( n = 6 per group). E Representative images of IHC staining of paraffin sections of in situ transplanted tumors in mice for Rab32, MMP2, MMP9, Vimentin N-cadherin, and E-cadherin. Scale bars = 100 μm. F Western blot analysis of Rab32, MMP2, MMP9, N-cadherin, E-cadherin, and Vimentin in situ xenograft tumors derived from NC- or Rab32 silenced -U87 cells. G Western blot analysis of Rab32, p-ERK 1/2 , ERK 1/2, p-Drp1 S616 , p-Drp1 S637 and Drp1 in xenograft tumors derived from NC- or Rab32 silenced -U87 cells. β-Actin was used as loading control. All data are shown as the mean ± SD of three replicates. ** P < 0.01, *** P < 0.001.

    Techniques Used: Injection, In Situ, Transfection, Immunohistochemistry, Western Blot, Derivative Assay

    rabbit monoclonal anti e cadherin antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit monoclonal anti e cadherin antibody
    Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of <t>E-cadherin</t> in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.
    Rabbit Monoclonal Anti E Cadherin Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Correlation between Macrophage Polarization and PD-L1-Related Tumor Microenvironmental Alteration and Metastasis in Pancreatic Ductal Adenocarcinoma"

    Article Title: Correlation between Macrophage Polarization and PD-L1-Related Tumor Microenvironmental Alteration and Metastasis in Pancreatic Ductal Adenocarcinoma

    Journal: Journal of Oncology

    doi: 10.1155/2023/7971306

    Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of E-cadherin in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.
    Figure Legend Snippet: Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of E-cadherin in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.

    Techniques Used: Immunohistochemistry, Immunohistochemical staining

    Relationship between E-cadherin, N-cadherin. and clinicopathological parameters in 42 primary tumors of PDAC.
    Figure Legend Snippet: Relationship between E-cadherin, N-cadherin. and clinicopathological parameters in 42 primary tumors of PDAC.

    Techniques Used: Expressing

    Spearman correlation analysis between the number of M2 macrophages infiltration in metastatic site and EMT markers. (a) There was no significant correlation between the number of M2 macrophages infiltration and E-cadherin in metastases. (b) Significant correlation was found between the number of M2 macrophages infiltration and E-cadherin in metastatic site.
    Figure Legend Snippet: Spearman correlation analysis between the number of M2 macrophages infiltration in metastatic site and EMT markers. (a) There was no significant correlation between the number of M2 macrophages infiltration and E-cadherin in metastases. (b) Significant correlation was found between the number of M2 macrophages infiltration and E-cadherin in metastatic site.

    Techniques Used:

    e cadherin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc e cadherin
    Immunofluorescence images of ( a ) PIN1, ( b ) <t>E-cadherin,</t> ( c ) N-cadherin and ( d ) HIF1-α in lung tissue after different treatments.
    E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Nanocarrier of Pin1 inhibitor based on supercritical fluid technology inhibits cancer metastasis by blocking multiple signaling pathways"

    Article Title: Nanocarrier of Pin1 inhibitor based on supercritical fluid technology inhibits cancer metastasis by blocking multiple signaling pathways

    Journal: Regenerative Biomaterials

    doi: 10.1093/rb/rbad014

    Immunofluorescence images of ( a ) PIN1, ( b ) E-cadherin, ( c ) N-cadherin and ( d ) HIF1-α in lung tissue after different treatments.
    Figure Legend Snippet: Immunofluorescence images of ( a ) PIN1, ( b ) E-cadherin, ( c ) N-cadherin and ( d ) HIF1-α in lung tissue after different treatments.

    Techniques Used: Immunofluorescence

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    • e cadherin  (Cell Signaling Technology Inc)
    86
    Cell Signaling Technology Inc e cadherin
    (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in <t>E-cadherin,</t> N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.
    E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti e cadherin  (Cell Signaling Technology Inc)
    86
    Cell Signaling Technology Inc anti e cadherin
    Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and <t>E-cadherin</t> or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.
    Anti E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    antibodies against e cadherin  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc antibodies against e cadherin
    (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of <t>E-cadherin</t> (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.
    Antibodies Against E Cadherin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit monoclonal anti e cadherin antibody  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc rabbit monoclonal anti e cadherin antibody
    Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of <t>E-cadherin</t> in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.
    Rabbit Monoclonal Anti E Cadherin Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in E-cadherin, N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.

    Journal: Journal of Clinical and Translational Hepatology

    Article Title: STX5 Inhibits Hepatocellular Carcinoma Adhesion and Promotes Metastasis by Regulating the PI3K/mTOR Pathway

    doi: 10.14218/JCTH.2022.00276

    Figure Lengend Snippet: (A) qPCR of basal STX5 mRNA expression in five cell lines. (B) Western blot analysis of basal STX5 protein expression in the five cell lines. (C-D) qPCR of STX5 mRNA expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and negative control LV-NC for 24 h. (E) qPCR of STX5 mRNA expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (F-G) Western blot analysis of STX5 protein expression in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and the LV-NC negative control for 24. (H) Western blot analysis of STX5 protein expression in MHCC97H cells transduced with OE-STX5 and negative control vector for 24 h. (I) Colony formation assay of the growth of Huh7 cells transduced with LV-shSTX5 and the negative control LV-NC over a 2-week period. (J-K) Detection of changes in E-cadherin, N-cadherin, and Snail protein levels in Huh7 and PLC/PRF/5 cells transduced with LV-shSTX5 and LV-NC and in MHCC97H cells transfected with OE-STX5 and the vector. (L-N) Comparison of migration in Huh7, PLC/PRF/5, and MHCC97H cells using Transwell chambers. (O-P) Comparison of the adhesion of Huh7, PLC/PRF/5, and MHCC97H cells to the extracellular matrix. (Q-S) Wound healing assays to compare the motility of the Huh7, PLC/PRF/5, and MHCC97H cell lines. Data are means ± SD of three independent assays. * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001. qPCR, quantitative polymerase chain reaction; EMT, epithelial-mesenchymal transition.

    Article Snippet: The primary antibodies were anti-p-PI3K, PI3K, mTOR, E-cadherin, N-cadherin, Vimentin, Snail, and GAPDH (Cell Signaling Technology, Danvers, MA, USA), and anti-STX5 (Abcam, Cambridge, UK).

    Techniques: Expressing, Western Blot, Transduction, Negative Control, Plasmid Preparation, Colony Assay, Transfection, Migration, Real-time Polymerase Chain Reaction

    Nude mice ( n =5) were injected with 2 × 10 6 LV-shNC or LV-shSTX5 Huh7 cells suspended in 200 µL of PBS via the tail vein. (A) Representative images of hepatic tissues from nude mice. (B) Representative images of lung tissues from nude mice. (C) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in lung tissue. (D) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in liver tissue. AFP, alpha-fetoprotein; IHC, immunohistochemical.

    Journal: Journal of Clinical and Translational Hepatology

    Article Title: STX5 Inhibits Hepatocellular Carcinoma Adhesion and Promotes Metastasis by Regulating the PI3K/mTOR Pathway

    doi: 10.14218/JCTH.2022.00276

    Figure Lengend Snippet: Nude mice ( n =5) were injected with 2 × 10 6 LV-shNC or LV-shSTX5 Huh7 cells suspended in 200 µL of PBS via the tail vein. (A) Representative images of hepatic tissues from nude mice. (B) Representative images of lung tissues from nude mice. (C) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in lung tissue. (D) Hematoxylin and eosin and IHC staining of AFP, STX5, E-cadherin, and N-cadherin in liver tissue. AFP, alpha-fetoprotein; IHC, immunohistochemical.

    Article Snippet: The primary antibodies were anti-p-PI3K, PI3K, mTOR, E-cadherin, N-cadherin, Vimentin, Snail, and GAPDH (Cell Signaling Technology, Danvers, MA, USA), and anti-STX5 (Abcam, Cambridge, UK).

    Techniques: Injection, Immunohistochemistry, Immunohistochemical staining

    Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and E-cadherin or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.

    Journal: The Journal of Cell Biology

    Article Title: Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer

    doi: 10.1083/jcb.202203036

    Figure Lengend Snippet: Transient expression of Prdm16 during PDAC progression. (A) Kaplan-Meier survival analysis of control, KSC, KIC, and KPC mice ( n = 31–39). Statistical power was assessed by a log-rank test for significance. (B) FFPE pancreatic sections from 4-mo-old control and KIC mice ( n = 38–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (C) FFPE pancreatic sections from 3-mo-old control and KPC mice ( n = 31–39) were stained with H&E or immunostained with anti-Prdm16 antibody and subjected to IHC. Representative pictures of normal, PanIN, and PDAC areas are shown. Scale bars: 50 μm (left). Relative Prdm16 expression in normal tissue and PanIN or PDAC lesions are shown (right). Data are expressed as mean ± SEM. (D) FFPE pancreatic sections from control and KSC mice ( n = 31–45) were subjected to co-IF using antibodies to Prdm16 and E-cadherin or vimentin. Representative pictures of normal tissue and IPMN or PDAC areas are shown. Scale bars: 50 μm. (E) Kaplan-Meier survival analysis of patients with wild-type or mutated SMAD4 based on high versus low PRDM16 expression was conducted using the TCGA dataset. Statistical power was assessed by log-rank test for significance. Statistical power in B and C were assessed by a two-tailed, unpaired Mann–Whitney test.

    Article Snippet: Chromatin immunoprecipitation (ChIP), immunoblotting, immunofluorescence, or immunohistochemistry were performed using the following antibodies: anti-α-SMA (#19245T; Cell Signaling); anti-β-Actin (#64225332; Bio-Rad), anti-amylase (#ab21156; Abcam), anti-chromogranin-A (#ab45179; Abcam), anti-cytokeratin 19 (#ab52625; Abcam), anti-E-cadherin (#3195S; Cell Signaling), anti-glucagon (#2760; Cell Signaling), anti-insulin (#4590; Cell Signaling), anti-JunB (#3753; Cell Signaling), anti-Muc5AC (#ab3649; Abcam), anti-Prdm16 (#ab202344 and #ab106410; Abcam), anti-Smad2 (#5339; Cell Signaling), anti-Smad3, (#9523; Cell Signaling), anti-Smad4, (#46535; Cell Signaling), anti-Smad4 (#sc-7966; Santa Cruz), anti-Smad2/3 (#8685; Cell Signaling), and anti-vimentin (#5741S; Cell Signaling).

    Techniques: Expressing, Staining, Two Tailed Test, MANN-WHITNEY

    Prdm16 inactivation in KSC mice resulted in acceleration of PDAC. (A) FFPE pancreatic sections from 4-mo-old control, KC, KPrC, KSC, and KSPrC mice ( n = 13–45) were stained with H&E or Alcian blue or immunostained with antibodies to CK19 or Muc5AC and subjected to IHC. Relative abundance of IPMN lesions (top left) or intensity of CK19 (top right), Muc5AC (bottom left), or Alcian blue (bottom right) are shown. Data are expressed as mean ± SEM, and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test. (B) FFPE pancreatic sections from control, KPrC, KSC, and KSPrC mice ( n = 13–45) were subjected to IF using antibodies to E-cadherin or vimentin. Representative pictures are shown. Scale bars: 50 μm. (C) Pictures of tumors harvested from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA ( n = 3). (D) FFPE liver and lung sections from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA were stained with H&E ( n = 3). Representative pictures are shown. Scale bars: 50 μm. (E) Representative pictures of soft-agar colonies formed by isogenic PANC-1 cell lines stably expressing control or PRDM16 gRNA. BxPC-3 stably expressing control or PRDM16 gRNA did not form colonies. (F) Cell proliferation assay of isogenic PANC-1 (day 3) and BxPC-3 (day 6) cell lines stably expressing control or PRDM16 gRNA. The fold increase in cell number at the end of the experiment relative to the seeding density is shown ( n = 3). Data are expressed as mean ± SEM and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test.

    Journal: The Journal of Cell Biology

    Article Title: Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer

    doi: 10.1083/jcb.202203036

    Figure Lengend Snippet: Prdm16 inactivation in KSC mice resulted in acceleration of PDAC. (A) FFPE pancreatic sections from 4-mo-old control, KC, KPrC, KSC, and KSPrC mice ( n = 13–45) were stained with H&E or Alcian blue or immunostained with antibodies to CK19 or Muc5AC and subjected to IHC. Relative abundance of IPMN lesions (top left) or intensity of CK19 (top right), Muc5AC (bottom left), or Alcian blue (bottom right) are shown. Data are expressed as mean ± SEM, and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test. (B) FFPE pancreatic sections from control, KPrC, KSC, and KSPrC mice ( n = 13–45) were subjected to IF using antibodies to E-cadherin or vimentin. Representative pictures are shown. Scale bars: 50 μm. (C) Pictures of tumors harvested from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA ( n = 3). (D) FFPE liver and lung sections from NSG mice injected with isogenic PANC-1 and BxPC-3 cell lines stably expressing control or PRDM16 gRNA were stained with H&E ( n = 3). Representative pictures are shown. Scale bars: 50 μm. (E) Representative pictures of soft-agar colonies formed by isogenic PANC-1 cell lines stably expressing control or PRDM16 gRNA. BxPC-3 stably expressing control or PRDM16 gRNA did not form colonies. (F) Cell proliferation assay of isogenic PANC-1 (day 3) and BxPC-3 (day 6) cell lines stably expressing control or PRDM16 gRNA. The fold increase in cell number at the end of the experiment relative to the seeding density is shown ( n = 3). Data are expressed as mean ± SEM and statistical power was assessed by a two-tailed, unpaired Mann–Whitney test.

    Article Snippet: Chromatin immunoprecipitation (ChIP), immunoblotting, immunofluorescence, or immunohistochemistry were performed using the following antibodies: anti-α-SMA (#19245T; Cell Signaling); anti-β-Actin (#64225332; Bio-Rad), anti-amylase (#ab21156; Abcam), anti-chromogranin-A (#ab45179; Abcam), anti-cytokeratin 19 (#ab52625; Abcam), anti-E-cadherin (#3195S; Cell Signaling), anti-glucagon (#2760; Cell Signaling), anti-insulin (#4590; Cell Signaling), anti-JunB (#3753; Cell Signaling), anti-Muc5AC (#ab3649; Abcam), anti-Prdm16 (#ab202344 and #ab106410; Abcam), anti-Smad2 (#5339; Cell Signaling), anti-Smad3, (#9523; Cell Signaling), anti-Smad4, (#46535; Cell Signaling), anti-Smad4 (#sc-7966; Santa Cruz), anti-Smad2/3 (#8685; Cell Signaling), and anti-vimentin (#5741S; Cell Signaling).

    Techniques: Staining, Two Tailed Test, MANN-WHITNEY, Injection, Stable Transfection, Expressing, Proliferation Assay

    (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.

    Journal: bioRxiv

    Article Title: High prevalence and dependence of centrosome clustering in mesenchymal tumors and leukemia

    doi: 10.1101/2023.03.13.532472

    Figure Lengend Snippet: (A) Barplot showing gene sets whose down or up-regulation is significantly associated with CC (FDR < 0.05). Gene Set Enrichment Analysis (GSEA) was done on genes ranked by the t-statistic of association with CC linearly modeled as per the equation shown and described in (Table 2). Ribosomal gene sets, of which several were upregulated, and general extracellular matrix gene sets, of which several were downregulated, were omitted to improve visualization and as they are frequently falsely enriched due to gene-length bias ( Mandelboum et al , 2019 ). (B, C) GSEA results for a mesenchymal (B) (MESENCHYMAL_ROKAVEC_CCLE) and an epithelial (C) (EPITHELIAL_ROKAVEC_CCLE) gene set with genes ranked by their association with CC in the linear model (Table 3). The results indicate a positive association of mesenchymal and a negative association of epithelial genes with CC. GSEA p-values are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (D, E) Volcano plots of differential gene expression associated with CC. Genes that belong to the mesenchymal (D) and the epithelial (E) gene sets in (B,C) are highlighted according to whether they are significantly negatively (blue) or positively (red) associated with CC. One of our top upregulated mesenchymal gene ANXA5, has been shown to promote epithelial-mesenchymal transition (EMT) in renal cancer ( Tang et al , 2017 ) and JUP, the top downregulated epithelial gene found, is an important component of intercellular junctions, which help hold neighboring cells together thus inhibiting cell spreading, invasion and metastases ( Aktary et al , 2017 ). (F) Representative images showing the effect of the treatment of HS578T cells with TGFβ (6 days). (G) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh), upregulation of Fibronectin (FN), N-cadherin (N-cadh) and Vimentin (Vim)) in control cells (MCF7 -full epithelial cell line) and in HS578T cells treated with and without TGFβ for 6 days. GAPDH level was used to normalize the amount of protein loaded per lane. (H) Percentage of mitotic cells assemblying bipolar spindles, formed either by CC or by alternative mechanisms (Extrusion, inactivation or the combination of both), and cells showing multipolar spindles in HS578T control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n=3)). Quantifications were performed at the end of the 6 days in both conditions. Significant p-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA for changes in the % of cells undergoing clustering and multipolar spindles between control conditions and the TGFβ treatment are *** p= 0.0009 and ** p= 0.0094 respectively. The total percentage of CA is also annotated in both conditions. (I) Representative images showing the effect of TGFβ treatment (6 days) in MCF10A-iPlk4 cells (I). (J) Flowchart summarizing the experiments designed to test the effect of the EMT in CC efficiency in MCF10A-iPLK4. (K) Representative Western Blot analysis showing main EMT markers (loss of E-cadherin (E-cadh) and upregulation of Fibronectin (FN), and Vimentin (Vim)) in the presence or absence of TGFβ treatment conjugated with PLK4 expression induced with doxycycline in MCF10A-iPlk4 cell line. GAPDH level was used to normalize the amount of protein loaded per lane. (L) Percentage of mitotic cells with bipolar spindles, formed either by CC (red) or alternative mechanisms (Extrusion, inactivation or the combination of both) (blue), and multipolar spindles (grey) in MCF10A-iPLK4 control cells and treated with TGFβ for 6 days (A minimum of 50 cells with CA were counted per experiment (n = 3). CA (%) scored in MCF10A-iPLK4 in control conditions (nothing added), treated either with doxycycline or TGFβ alone or the combination of both (Doxycycline + TGFβ) are shown. Quantifications were performed at the end of the 6 days in all the conditions. Note that the level of CA is higher than usual in basal conditions probably caused over time by leaky Plk4-expression in the absence of doxycycline. Significant P-values derived from Tukey’s multiple comparisons test performed by two-way ANOVA are the following: Clustering : **** p< 0.0001 for Control vs. TGFβ; *** p= 0.0002 for Control vs. TGFβ-Dox; *** p= 0.0001 for Control-Dox vs. TGFβ, *** p= 0.0005 for Control-Dox vs. TGFβ-Dox; *** p ≤ 0.0005. Multipolar : ** p=0.0019 for Control vs. TGFβ; **** p<0.0001 for Control-Dox vs. TGFβ; *** p=0.0002 for Control-Dox vs. TGFβ-Dox. Alternative mechanisms : * p=0.0386 Control vs. Control-Dox. Images show the DNA in cyan, centrioles in green (Centrin-2) and red (CP110), and the spindle in magenta (α-Tubulin). Scale bar 5 μm, insets 1 μm.

    Article Snippet: Immunodetection was performed by incubation with antibodies against E-cadherin (1:1000; 3195S from Cell signaling), Vimentin (1:250; sc-373717), fibronectin (1:250; sc-18825) and N-cadherin (1:200; sc-59987) from Santa Cruz Biotechnology.

    Techniques: Expressing, Western Blot, Derivative Assay

    (A) GSEA of centriole-associated gene sets with genes ranked by their association with CC in the linear model. GSEA peak enrichment scores (ES) and false discovery rates (FDR) are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (B) Volcano plots of differential gene expression associated with CC. Genes that belong to the gene sets in (A) are highlighted according to whether they are negatively (blue) or positively (red) associated with CC. (C) Barplot showing GSEA enrichment scores for all gene sets comprising mesenchymal or epithelial genes. The FDR was calculated using the full set of gene sets used in this study. Gene sets with significant genes over or under-expressed in association with CC (FDR < 0.05) are represented in red and blue, respectively. (D) T-statistic for association of protein expression with CC, linearly modelled according to the equation at the top using three independent datasets ( Gholami et al , 2013 ; Nishizuka et al , 2003 ; Guo et al , 2019 ) shows consistent, albeit not significant, negative association of E-cadherin (CDH1), β-catenin (CTNNB1) and PDLIM1 levels with CC (Table 1). PDLIM1 downregulation has been associated with metastatic potential in colorectal cancer through destabilization of the E-cadherin/β-catenin complex ( Chen et al , 2016 )

    Journal: bioRxiv

    Article Title: High prevalence and dependence of centrosome clustering in mesenchymal tumors and leukemia

    doi: 10.1101/2023.03.13.532472

    Figure Lengend Snippet: (A) GSEA of centriole-associated gene sets with genes ranked by their association with CC in the linear model. GSEA peak enrichment scores (ES) and false discovery rates (FDR) are shown. Genes are ranked by their t-statistic of association with CC and plotted on the X-axis. Genes that belong to the gene set of interest are indicated by vertical black bars. The enrichment score is plotted in green. (B) Volcano plots of differential gene expression associated with CC. Genes that belong to the gene sets in (A) are highlighted according to whether they are negatively (blue) or positively (red) associated with CC. (C) Barplot showing GSEA enrichment scores for all gene sets comprising mesenchymal or epithelial genes. The FDR was calculated using the full set of gene sets used in this study. Gene sets with significant genes over or under-expressed in association with CC (FDR < 0.05) are represented in red and blue, respectively. (D) T-statistic for association of protein expression with CC, linearly modelled according to the equation at the top using three independent datasets ( Gholami et al , 2013 ; Nishizuka et al , 2003 ; Guo et al , 2019 ) shows consistent, albeit not significant, negative association of E-cadherin (CDH1), β-catenin (CTNNB1) and PDLIM1 levels with CC (Table 1). PDLIM1 downregulation has been associated with metastatic potential in colorectal cancer through destabilization of the E-cadherin/β-catenin complex ( Chen et al , 2016 )

    Article Snippet: Immunodetection was performed by incubation with antibodies against E-cadherin (1:1000; 3195S from Cell signaling), Vimentin (1:250; sc-373717), fibronectin (1:250; sc-18825) and N-cadherin (1:200; sc-59987) from Santa Cruz Biotechnology.

    Techniques: Expressing

    Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of E-cadherin in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.

    Journal: Journal of Oncology

    Article Title: Correlation between Macrophage Polarization and PD-L1-Related Tumor Microenvironmental Alteration and Metastasis in Pancreatic Ductal Adenocarcinoma

    doi: 10.1155/2023/7971306

    Figure Lengend Snippet: Immunohistochemistry and quantification of EMT markers in in primary tumors and metastatic site. (a) Representative immunohistochemical image of E-cadherin in primary tumors and metastatic site. (b) Representative immunohistochemical image of ZEB1 in primary tumors and metastatic site. (c) Representative immunohistochemical image of N-cadherin in primary tumors and metastatic site. (d) Representative immunohistochemical image of Snail in primary tumors and metastatic site. ∗∗∗ P < 0.001; ns, not significant.

    Article Snippet: The following antibodies were used: rabbit monoclonal anti-CD86 antibody (Cell Signaling Technology Cat# 91882), rabbit monoclonal anti-CD163 antibody (Gene Tech Cat# GT2077), rabbit monoclonal anti-PD-L1 antibody (Cell Signaling Technology Cat# 13684), rabbit monoclonal anti-E-cadherin antibody (Gene Tech Cat# GT210702), rabbit monoclonal anti-N-cadherin antibody (Cell Signaling Technology Cat# 13116), rabbit monoclonal anti-ZEB1 antibody (Cell Signaling Technology Cat# 70512), and rabbit polyclonal anti-Snail antibody (HuaBio, Cat# ER1706-22).

    Techniques: Immunohistochemistry, Immunohistochemical staining

    Relationship between E-cadherin, N-cadherin. and clinicopathological parameters in 42 primary tumors of PDAC.

    Journal: Journal of Oncology

    Article Title: Correlation between Macrophage Polarization and PD-L1-Related Tumor Microenvironmental Alteration and Metastasis in Pancreatic Ductal Adenocarcinoma

    doi: 10.1155/2023/7971306

    Figure Lengend Snippet: Relationship between E-cadherin, N-cadherin. and clinicopathological parameters in 42 primary tumors of PDAC.

    Article Snippet: The following antibodies were used: rabbit monoclonal anti-CD86 antibody (Cell Signaling Technology Cat# 91882), rabbit monoclonal anti-CD163 antibody (Gene Tech Cat# GT2077), rabbit monoclonal anti-PD-L1 antibody (Cell Signaling Technology Cat# 13684), rabbit monoclonal anti-E-cadherin antibody (Gene Tech Cat# GT210702), rabbit monoclonal anti-N-cadherin antibody (Cell Signaling Technology Cat# 13116), rabbit monoclonal anti-ZEB1 antibody (Cell Signaling Technology Cat# 70512), and rabbit polyclonal anti-Snail antibody (HuaBio, Cat# ER1706-22).

    Techniques: Expressing

    Spearman correlation analysis between the number of M2 macrophages infiltration in metastatic site and EMT markers. (a) There was no significant correlation between the number of M2 macrophages infiltration and E-cadherin in metastases. (b) Significant correlation was found between the number of M2 macrophages infiltration and E-cadherin in metastatic site.

    Journal: Journal of Oncology

    Article Title: Correlation between Macrophage Polarization and PD-L1-Related Tumor Microenvironmental Alteration and Metastasis in Pancreatic Ductal Adenocarcinoma

    doi: 10.1155/2023/7971306

    Figure Lengend Snippet: Spearman correlation analysis between the number of M2 macrophages infiltration in metastatic site and EMT markers. (a) There was no significant correlation between the number of M2 macrophages infiltration and E-cadherin in metastases. (b) Significant correlation was found between the number of M2 macrophages infiltration and E-cadherin in metastatic site.

    Article Snippet: The following antibodies were used: rabbit monoclonal anti-CD86 antibody (Cell Signaling Technology Cat# 91882), rabbit monoclonal anti-CD163 antibody (Gene Tech Cat# GT2077), rabbit monoclonal anti-PD-L1 antibody (Cell Signaling Technology Cat# 13684), rabbit monoclonal anti-E-cadherin antibody (Gene Tech Cat# GT210702), rabbit monoclonal anti-N-cadherin antibody (Cell Signaling Technology Cat# 13116), rabbit monoclonal anti-ZEB1 antibody (Cell Signaling Technology Cat# 70512), and rabbit polyclonal anti-Snail antibody (HuaBio, Cat# ER1706-22).

    Techniques: