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Abcam antibody ki 67
Down-regulated ZFAS1 or up-regulated miR-135a restrains colony formation ability and proliferation of MG63 cells. A The colony formation ability of MG63 cells in each group. B Quantification results in A . C MG63 cell proliferation tested by MTT assay. D EdU assay for detecting proliferation of MG63 cells. E Quantification results in D . F <t>Ki-67</t> and CyclinD1 protein band and expression in each group of MG63 cells. The data in the figure were all measurement data, in the form of mean ± standard deviation; a vs the sh-NC group, P
Antibody Ki 67, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Silencing lncRNA ZFAS1 or elevated microRNA-135a represses proliferation, migration, invasion and resistance to apoptosis of osteosarcoma cells"

Article Title: Silencing lncRNA ZFAS1 or elevated microRNA-135a represses proliferation, migration, invasion and resistance to apoptosis of osteosarcoma cells

Journal: Cancer Cell International

doi: 10.1186/s12935-019-1049-x

Down-regulated ZFAS1 or up-regulated miR-135a restrains colony formation ability and proliferation of MG63 cells. A The colony formation ability of MG63 cells in each group. B Quantification results in A . C MG63 cell proliferation tested by MTT assay. D EdU assay for detecting proliferation of MG63 cells. E Quantification results in D . F Ki-67 and CyclinD1 protein band and expression in each group of MG63 cells. The data in the figure were all measurement data, in the form of mean ± standard deviation; a vs the sh-NC group, P
Figure Legend Snippet: Down-regulated ZFAS1 or up-regulated miR-135a restrains colony formation ability and proliferation of MG63 cells. A The colony formation ability of MG63 cells in each group. B Quantification results in A . C MG63 cell proliferation tested by MTT assay. D EdU assay for detecting proliferation of MG63 cells. E Quantification results in D . F Ki-67 and CyclinD1 protein band and expression in each group of MG63 cells. The data in the figure were all measurement data, in the form of mean ± standard deviation; a vs the sh-NC group, P

Techniques Used: MTT Assay, EdU Assay, Expressing, Standard Deviation

2) Product Images from "Deoxyelephantopin Suppresses Pancreatic Cancer Progression In Vitro and In Vivo by Targeting linc00511/miR-370-5p/p21 Promoter Axis"

Article Title: Deoxyelephantopin Suppresses Pancreatic Cancer Progression In Vitro and In Vivo by Targeting linc00511/miR-370-5p/p21 Promoter Axis

Journal: Journal of Oncology

doi: 10.1155/2022/3855462

The effect of linc00511 on tumorigenesis and DET sensitivity in vivo . (a) Xenograft tumor model was obtained by subcutaneous injection of BxPC-3 cells transfected with pcDNA3.1-linc00511 or empty vector. ( n = 5). (b) The detailed grouping strategies and intervention measures of xenograft model. (c) The curves of tumor volume in nude mice were plotted using measurements obtained every 3 days. (d) After 33 days of subcutaneous injection, complete resections were performed to obtain the tumors from the nude mice, and the more precise final tumor volume was assessed. (e) The final tumor weight was measured. (f) IHC staining targeting Ki-67, PCNA, and E-cadherin was carried out; meanwhile, the corresponding quantitative statistics were shown. (g) Lung metastatic tumor model was established by tail vein injection, and the HE staining was performed to identify the histopathological changes. ( n = 4). ∗ P
Figure Legend Snippet: The effect of linc00511 on tumorigenesis and DET sensitivity in vivo . (a) Xenograft tumor model was obtained by subcutaneous injection of BxPC-3 cells transfected with pcDNA3.1-linc00511 or empty vector. ( n = 5). (b) The detailed grouping strategies and intervention measures of xenograft model. (c) The curves of tumor volume in nude mice were plotted using measurements obtained every 3 days. (d) After 33 days of subcutaneous injection, complete resections were performed to obtain the tumors from the nude mice, and the more precise final tumor volume was assessed. (e) The final tumor weight was measured. (f) IHC staining targeting Ki-67, PCNA, and E-cadherin was carried out; meanwhile, the corresponding quantitative statistics were shown. (g) Lung metastatic tumor model was established by tail vein injection, and the HE staining was performed to identify the histopathological changes. ( n = 4). ∗ P

Techniques Used: In Vivo, Injection, Transfection, Plasmid Preparation, Mouse Assay, Immunohistochemistry, Staining

Silence of linc00511 enhanced the inhibitory effect of DET on tumor cell proliferation, migration, and invasion. (a) BxPC-3 and CFPAC-1 cells were transfected with si-NC or specific siRNAs targeting linc00511, and the knockdown efficiency was measured by qRT-PCR. (b) The cell viability of BxPC-3 and CFPAC-1 cells after siRNAs transfection was evaluated by CCK-8 assays. (c) The effect of DET treatment combined siRNAs transfection on cell viability was also detected by CCK-8 assays. (d) The location and expression level of Ki-67 in BxPC-3 and CFPAC-1 cells after silencing linc00511 or treating with DET were examined by IF. (e) The proliferation of BxPC-3 and CFPAC-1 cells after DET treatment, siRNAs transfection, or combined stimulation was assessed by colony formation experiments. (f-g) The mobility of BxPC-3 and CFPAC-1 cells after different stimulation was examined by wound healing assays. (h-i) The migration and invasion abilities of BxPC-3 and CFPAC-1 cells after different stimulation were assessed by Transwell assays. ∗∗ P
Figure Legend Snippet: Silence of linc00511 enhanced the inhibitory effect of DET on tumor cell proliferation, migration, and invasion. (a) BxPC-3 and CFPAC-1 cells were transfected with si-NC or specific siRNAs targeting linc00511, and the knockdown efficiency was measured by qRT-PCR. (b) The cell viability of BxPC-3 and CFPAC-1 cells after siRNAs transfection was evaluated by CCK-8 assays. (c) The effect of DET treatment combined siRNAs transfection on cell viability was also detected by CCK-8 assays. (d) The location and expression level of Ki-67 in BxPC-3 and CFPAC-1 cells after silencing linc00511 or treating with DET were examined by IF. (e) The proliferation of BxPC-3 and CFPAC-1 cells after DET treatment, siRNAs transfection, or combined stimulation was assessed by colony formation experiments. (f-g) The mobility of BxPC-3 and CFPAC-1 cells after different stimulation was examined by wound healing assays. (h-i) The migration and invasion abilities of BxPC-3 and CFPAC-1 cells after different stimulation were assessed by Transwell assays. ∗∗ P

Techniques Used: Migration, Transfection, Quantitative RT-PCR, CCK-8 Assay, Expressing

Linc00511 overexpression attenuated the suppressive effect of DET on tumor cell proliferation, migration, and invasion (a) BxPC-3 and CFPAC-1 cells were transfected with pcDNA3.1-linc00511 or corresponding empty vector, and the overexpression efficiency was analyzed by qRT-PCR. (b) The effect of linc00511 overexpression on cell viability was assessed by CCK-8 assays. (c) The effect of DET treatment combined pcDNA3.1-linc00511 transfection on cell viability was similarly detected by CCK-8 assays. (d) The location and expression of Ki-67 in cells after linc00511 overexpression or DET treatment were examined by IF. (e) The proliferation of BxPC-3 and CFPAC-1 cells after DET treatment, pcDNA3.1 transfection, or combined treatment was evaluated by colony formation assays. (f-g) The mobility of BxPC-3 and CFPAC-1 cells after different stimulation was estimated by wound healing assays. (h-i) The cell migration and invasion abilities after different treatment were detected by Transwell assays. ∗ P
Figure Legend Snippet: Linc00511 overexpression attenuated the suppressive effect of DET on tumor cell proliferation, migration, and invasion (a) BxPC-3 and CFPAC-1 cells were transfected with pcDNA3.1-linc00511 or corresponding empty vector, and the overexpression efficiency was analyzed by qRT-PCR. (b) The effect of linc00511 overexpression on cell viability was assessed by CCK-8 assays. (c) The effect of DET treatment combined pcDNA3.1-linc00511 transfection on cell viability was similarly detected by CCK-8 assays. (d) The location and expression of Ki-67 in cells after linc00511 overexpression or DET treatment were examined by IF. (e) The proliferation of BxPC-3 and CFPAC-1 cells after DET treatment, pcDNA3.1 transfection, or combined treatment was evaluated by colony formation assays. (f-g) The mobility of BxPC-3 and CFPAC-1 cells after different stimulation was estimated by wound healing assays. (h-i) The cell migration and invasion abilities after different treatment were detected by Transwell assays. ∗ P

Techniques Used: Over Expression, Migration, Transfection, Plasmid Preparation, Quantitative RT-PCR, CCK-8 Assay, Expressing

3) Product Images from "Liver-specific LINC01146, a promising prognostic indicator, inhibits the malignant phenotype of hepatocellular carcinoma cells both in vitro and in vivo"

Article Title: Liver-specific LINC01146, a promising prognostic indicator, inhibits the malignant phenotype of hepatocellular carcinoma cells both in vitro and in vivo

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-021-03225-2

Downregulation of LINC01146 promotes the tumour growth of HCC cells in vivo. A The results of HE and IHC staining of tumour tissues of nude mice. B Downregulation of LINC01146 promoted the positive expression of Ki-67 protein. **** P
Figure Legend Snippet: Downregulation of LINC01146 promotes the tumour growth of HCC cells in vivo. A The results of HE and IHC staining of tumour tissues of nude mice. B Downregulation of LINC01146 promoted the positive expression of Ki-67 protein. **** P

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

4) Product Images from "Eukaryotic Translation Initiation Factor 3 Subunit B Is a Promoter in the Development and Progression of Pancreatic Cancer"

Article Title: Eukaryotic Translation Initiation Factor 3 Subunit B Is a Promoter in the Development and Progression of Pancreatic Cancer

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2021.644156

Eukaryotic translation initiation factor 3 subunit B (EIF3B) knockdown suppressed pancreatic cancer (PC) growth in vivo . (A) A nude mice model of EIF3B knockdown was constructed. (B) The volume of tumors was tested from feeding to sacrifice. (C) The fluorescence intensity was obtained through injection of D-Luciferase before sacrificing the mice. (D) The weight of tumors was measured after sacrificing the mice. (E) The photograph of tumors was taken after removing tumors. (F) The value of Ki-67 was detected by immunohistochemistry (IHC) in tumor sections. Results are presented as mean ± SD. *** P
Figure Legend Snippet: Eukaryotic translation initiation factor 3 subunit B (EIF3B) knockdown suppressed pancreatic cancer (PC) growth in vivo . (A) A nude mice model of EIF3B knockdown was constructed. (B) The volume of tumors was tested from feeding to sacrifice. (C) The fluorescence intensity was obtained through injection of D-Luciferase before sacrificing the mice. (D) The weight of tumors was measured after sacrificing the mice. (E) The photograph of tumors was taken after removing tumors. (F) The value of Ki-67 was detected by immunohistochemistry (IHC) in tumor sections. Results are presented as mean ± SD. *** P

Techniques Used: In Vivo, Mouse Assay, Construct, Fluorescence, Injection, Luciferase, Immunohistochemistry

5) Product Images from "CircRNA ZNF609 promotes the growth and metastasis of thyroid cancer in vivo and in vitro by downregulating miR-514a-5p"

Article Title: CircRNA ZNF609 promotes the growth and metastasis of thyroid cancer in vivo and in vitro by downregulating miR-514a-5p

Journal: Bioengineered

doi: 10.1080/21655979.2022.2033015

Circ-ZNF609 facilitated tumor growth by down-regulating miR-514a-5p in vivo . (a-d) The tumor weight and volume of mice treated with sh-circ-ZNF609 in the presence or absence of miR-514a-5p inhibitor were observed and measured. (e-f) Levels of Ki-67 and PCNA in TPC-1 and IHH-4 cells transfected with sh-circ-ZNF609 in the presence or absence of miR-514a-5p inhibitor, assayed employing Western blotting. All experimental results are recorded in the form of mean ± SD. *P
Figure Legend Snippet: Circ-ZNF609 facilitated tumor growth by down-regulating miR-514a-5p in vivo . (a-d) The tumor weight and volume of mice treated with sh-circ-ZNF609 in the presence or absence of miR-514a-5p inhibitor were observed and measured. (e-f) Levels of Ki-67 and PCNA in TPC-1 and IHH-4 cells transfected with sh-circ-ZNF609 in the presence or absence of miR-514a-5p inhibitor, assayed employing Western blotting. All experimental results are recorded in the form of mean ± SD. *P

Techniques Used: In Vivo, Mouse Assay, Transfection, Western Blot

Inhibition of circ-ZNF609 inhibited the proliferation of thyroid cancer cells. (a) Relative expression of circ-ZNF609 in several TC cell lines and normal thyroid cell line Nthy-ori 3–1, examined with the application of qRT-PCR. (b) Relative expression of circ-ZNF609 in TPC-1 and IHH-4 cells following circ-ZNF609 knockdown. Cell proliferation of TPC-1 and IHH-4 transfected with sh-circ-ZNF609, assayed with the use of CCK-8 assay (c) and colony formation assay (d-e). (f) Ki-67 expression in TPC-1 and IHH-4 transfected with sh-circ-ZNF609, examined applying immunofluorescence staining. Original magnification: 200 × . (g) Levels of Ki-67 and PCNA in TPC-1 and IHH-4 transfected with sh-circ-ZNF609, tested utilizing Western blotting. All experimental results are recorded in the form of mean ± SD. *P
Figure Legend Snippet: Inhibition of circ-ZNF609 inhibited the proliferation of thyroid cancer cells. (a) Relative expression of circ-ZNF609 in several TC cell lines and normal thyroid cell line Nthy-ori 3–1, examined with the application of qRT-PCR. (b) Relative expression of circ-ZNF609 in TPC-1 and IHH-4 cells following circ-ZNF609 knockdown. Cell proliferation of TPC-1 and IHH-4 transfected with sh-circ-ZNF609, assayed with the use of CCK-8 assay (c) and colony formation assay (d-e). (f) Ki-67 expression in TPC-1 and IHH-4 transfected with sh-circ-ZNF609, examined applying immunofluorescence staining. Original magnification: 200 × . (g) Levels of Ki-67 and PCNA in TPC-1 and IHH-4 transfected with sh-circ-ZNF609, tested utilizing Western blotting. All experimental results are recorded in the form of mean ± SD. *P

Techniques Used: Inhibition, Expressing, Quantitative RT-PCR, Transfection, CCK-8 Assay, Colony Assay, Immunofluorescence, Staining, Western Blot

Circ-ZNF609 silencing inhibited tumor growth in vivo . (a-d) The tumor weight and volume of mice injected with sh-circ-ZNF609 were observed and measured. (e) Relative expression of circ-ZNF609 in tumor tissues, assayed through the way of qRT-PCR. (f) Immunohistochemistry experiments about Ki-67 in tumor tissue from the sh-circZNF609 mice. Original magnification: 200 × . (g-h) Levels of Ki-67 and PCNA in mice injected with TPC-1 and IHH-4 cells transfected with sh-circ-ZNF609, assessed with the adoption of Western blotting. All experimental results are recorded in the form of mean ± SD. *P
Figure Legend Snippet: Circ-ZNF609 silencing inhibited tumor growth in vivo . (a-d) The tumor weight and volume of mice injected with sh-circ-ZNF609 were observed and measured. (e) Relative expression of circ-ZNF609 in tumor tissues, assayed through the way of qRT-PCR. (f) Immunohistochemistry experiments about Ki-67 in tumor tissue from the sh-circZNF609 mice. Original magnification: 200 × . (g-h) Levels of Ki-67 and PCNA in mice injected with TPC-1 and IHH-4 cells transfected with sh-circ-ZNF609, assessed with the adoption of Western blotting. All experimental results are recorded in the form of mean ± SD. *P

Techniques Used: In Vivo, Mouse Assay, Injection, Expressing, Quantitative RT-PCR, Immunohistochemistry, Transfection, Western Blot

Circ-ZNF609 promotes cell growth and metastasis by down-regulating miR-514a-5p in TPC-1 and IHH-4 cells. (a) Cell proliferation assay employed the experiment of CCK-8. (b) Levels of Ki-67 and PCNA were assessed with the application of Western blot. (c) Cell migration evaluation was undertaken with the help of wound healing. Original magnification: 100 × . (d) Cell invasion experiment was carried out via the way of transwell. Original magnification: 100 × . (e) Levels of MMP2 and MMP9 was examined applying Western blotting. All experimental results are recorded in the form of mean ± SD. *P
Figure Legend Snippet: Circ-ZNF609 promotes cell growth and metastasis by down-regulating miR-514a-5p in TPC-1 and IHH-4 cells. (a) Cell proliferation assay employed the experiment of CCK-8. (b) Levels of Ki-67 and PCNA were assessed with the application of Western blot. (c) Cell migration evaluation was undertaken with the help of wound healing. Original magnification: 100 × . (d) Cell invasion experiment was carried out via the way of transwell. Original magnification: 100 × . (e) Levels of MMP2 and MMP9 was examined applying Western blotting. All experimental results are recorded in the form of mean ± SD. *P

Techniques Used: Proliferation Assay, CCK-8 Assay, Western Blot, Migration

6) Product Images from "Knockdown of MCM8 inhibits development and progression of bladder cancer in vitro and in vivo"

Article Title: Knockdown of MCM8 inhibits development and progression of bladder cancer in vitro and in vivo

Journal: Cancer Cell International

doi: 10.1186/s12935-021-01948-2

Loss-of-function of MCM8 attenuated cell proliferation and migration of bladder cancer cells. a The cell proliferation rate was evaluated in bladder cancer cell lines after transfection by the MTT assay. b The migration rate of cells was detected in bladder cancer cell lines after transfection by wound-healing assay. c The migration rate of cells was detected in bladder cancer cell lines after transfection by transwell assay. Results were presented as mean ± SD. *** P
Figure Legend Snippet: Loss-of-function of MCM8 attenuated cell proliferation and migration of bladder cancer cells. a The cell proliferation rate was evaluated in bladder cancer cell lines after transfection by the MTT assay. b The migration rate of cells was detected in bladder cancer cell lines after transfection by wound-healing assay. c The migration rate of cells was detected in bladder cancer cell lines after transfection by transwell assay. Results were presented as mean ± SD. *** P

Techniques Used: Migration, Transfection, MTT Assay, Wound Healing Assay, Transwell Assay

Loss-of-function of MCM8 curbed bladder cancer tumorigenesis. a A nude mice model of MCM8 knockdown was constructed. b The volume of tumors was tested from feeding to sacrifice. c The fluorescence intensity was obtained through injection of D-Luciferase before sacrificing the mice. d The weight of tumors was measured after sacrificing mice. e The photograph of tumors was taken after removing tumors. f The value of Ki-67 was detected by IHC in tumor sections. Magnification times: 400 × . Results were presented as mean ± SD. * P
Figure Legend Snippet: Loss-of-function of MCM8 curbed bladder cancer tumorigenesis. a A nude mice model of MCM8 knockdown was constructed. b The volume of tumors was tested from feeding to sacrifice. c The fluorescence intensity was obtained through injection of D-Luciferase before sacrificing the mice. d The weight of tumors was measured after sacrificing mice. e The photograph of tumors was taken after removing tumors. f The value of Ki-67 was detected by IHC in tumor sections. Magnification times: 400 × . Results were presented as mean ± SD. * P

Techniques Used: Mouse Assay, Construct, Fluorescence, Injection, Luciferase, Immunohistochemistry

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    Abcam anti ki67 antibody
    RSK-3 activates rpS6, but not autophagy, to regulate CSPCs proliferation. The proliferative ability of CSPCs from C57/BL6J mice after RSK-3 inhibitor (BI-D1870) and mTOR inhibitor (rapamycin) treatment detected by CCK-8 assay ( A ) and <t>Ki67</t> labeling ( B ). ( C,D ) Protein expression of RSK-3, p-RSK-3, mTOR, p-mTOR, p-rpS6 and rpS6 in CSPCs from C57/BL6J mice and the corresponding quantifications. ( E ) p-RSK-3, p-mTOR and LC3 immunolabeling in CSPCs from C57/BL6J mice. * p
    Anti Ki67 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    RSK-3 activates rpS6, but not autophagy, to regulate CSPCs proliferation. The proliferative ability of CSPCs from C57/BL6J mice after RSK-3 inhibitor (BI-D1870) and mTOR inhibitor (rapamycin) treatment detected by CCK-8 assay ( A ) and Ki67 labeling ( B ). ( C,D ) Protein expression of RSK-3, p-RSK-3, mTOR, p-mTOR, p-rpS6 and rpS6 in CSPCs from C57/BL6J mice and the corresponding quantifications. ( E ) p-RSK-3, p-mTOR and LC3 immunolabeling in CSPCs from C57/BL6J mice. * p

    Journal: Theranostics

    Article Title: RSK-3 promotes cartilage regeneration via interacting with rpS6 in cartilage stem/progenitor cells

    doi: 10.7150/thno.44875

    Figure Lengend Snippet: RSK-3 activates rpS6, but not autophagy, to regulate CSPCs proliferation. The proliferative ability of CSPCs from C57/BL6J mice after RSK-3 inhibitor (BI-D1870) and mTOR inhibitor (rapamycin) treatment detected by CCK-8 assay ( A ) and Ki67 labeling ( B ). ( C,D ) Protein expression of RSK-3, p-RSK-3, mTOR, p-mTOR, p-rpS6 and rpS6 in CSPCs from C57/BL6J mice and the corresponding quantifications. ( E ) p-RSK-3, p-mTOR and LC3 immunolabeling in CSPCs from C57/BL6J mice. * p

    Article Snippet: The cells and sections were then blocked with 5% bovine serum albumin (BSA, Sigma, USA) and incubated overnight with rabbit-anti Collagen X (Abcam, 1:200, ab58632), rabbit-anti MMP-13 (Abcam, 1:200, ab39012), rabbit-anti RSK-3 (Proteintech, 1:200, 14446-1-AP), rabbit-anti p-RSK-3 (RD systems, 1:200, AF893), rabbit-anti CD44 (Abcam, 1:200, ab157107), mouse-anti CD90 (Abcam, 1:200, ab225), or rabbit-anti Ki67 (Abcam, 1:200, ab15580) diluted in 3% BSA.

    Techniques: Mouse Assay, CCK-8 Assay, Labeling, Expressing, Immunolabeling

    Assessment of liver function. (a) Immunofluorescent staining of Ki67 and PCNA (both in red), with nuclei shown in blue. (b) The expression of CYP3A1 and the expression of ALB in the liver was evaluated by Western blot, and β -actin was used as an internal reference. (c) ALB and G6pase expression in the liver was evaluated by RT-qPCR, and GADPH was used as a housekeeping gene. Results are shown as fold changes compared to the model group. ∗ p

    Journal: Stem Cells International

    Article Title: The Effect of Vascular Endothelial Growth Factor on Bone Marrow Mesenchymal Stem Cell Engraftment in Rat Fibrotic Liver upon Transplantation

    doi: 10.1155/2019/5310202

    Figure Lengend Snippet: Assessment of liver function. (a) Immunofluorescent staining of Ki67 and PCNA (both in red), with nuclei shown in blue. (b) The expression of CYP3A1 and the expression of ALB in the liver was evaluated by Western blot, and β -actin was used as an internal reference. (c) ALB and G6pase expression in the liver was evaluated by RT-qPCR, and GADPH was used as a housekeeping gene. Results are shown as fold changes compared to the model group. ∗ p

    Article Snippet: Following a wash step (10 min), sections were blocked in serum for 30 min, followed by primary antibody incubation overnight at 4°C: anti-α -SMA (α -smooth muscle actin, 1 : 500, GB13044, Servicebio), anti-collagen III (1 : 200, ab7778, Abcam), anti-VEGF (1 : 200, ab39250, Abcam), anti-VCAM-1 (1 : 100, ab134047, Abcam), anti-PCNA (proliferating cell nuclear antigen, 1 : 1000, GB11010, Servicebio), and anti-Ki67 (1 : 1000, ab15580, Abcam).

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

    The association between P‐gp expression and TET1 and immunohistochemical analysis in xenograft tumor tissues. (A) Western blot analysis of TET1 and P‐gp expression in RG‐QBC939 cells transfected with TET1 gene or siRNA‐ TET1 . The results showed that compared with untreated cells, p‐gp expression remarkably decreased in cells with higher expression of TET1 and increased in cells with lower expression of TET1. The experiments were performed three times. (B) Nude mice were raised, divided equally and randomly into four groups, and subcutaneously inoculated with QBC939 and RG‐QBC939 in the backs. Two groups of mice were treated with 400 mg/kg gemcitabine at the first day when tumors reached a maximum size of 150 mm 3 and treated with 200 mg/kg gemcitabine at the eighth day and fifteenth day. The other two groups of mice were not treated with gemcitabine as control groups. Each mouse was weighed weekly, and mice were killed after 28 days (4 weeks) and necropsied. Tumor volume was monitored every week, and tumor weights were measured at the fourth week after mice were killed. (C) Tumors from the mice without treatment of chemotherapy had no significant differences in volume and weights between two groups. (D) After mice‐implanted CCA cells were treated with a conventional course of chemotherapy for 4 weeks, tumors, including the average tumor volume weekly and tumor weights derived from RG‐QBC939 cells, appeared larger than those in the other group. (E) Tumor tissues from QBC939 and RG‐QBC939 cells were immunohistochemically stained for Ki67. Ki67 expression was significantly higher in tumor tissues from mice with implanted RG‐QBC939 than that with implanted QBC939. Dots represent IHC score from 10 mice tumor tissues. The magnification is 200 times. (F) The expression of TET1 in tumors was immunohistochemically analyzed and the results showed that TET1 was expressed lowly in tumors derived from RG‐QBC939 cells. Dots represent IHC score from 10 mice tumor tissues. The magnification is 200 times. (G) Correlations between TET1 and P‐gp expression in cholangiocarcinoma tissues. The results suggested that expression of TET1 inversely correlated with P‐gp expression. The magnification is 200 times. The P ‐values represent the results of two‐tailed Student's t ‐test for two groups. Data were mean ±SD

    Journal: Cancer Medicine

    Article Title: Enhanced expression of ten‐eleven translocation 1 reverses gemcitabine resistance in cholangiocarcinoma accompanied by a reduction in P‐glycoprotein expression, et al. Enhanced expression of ten‐eleven translocation 1 reverses gemcitabine resistance in cholangiocarcinoma accompanied by a reduction in P‐glycoprotein expression

    doi: 10.1002/cam4.1983

    Figure Lengend Snippet: The association between P‐gp expression and TET1 and immunohistochemical analysis in xenograft tumor tissues. (A) Western blot analysis of TET1 and P‐gp expression in RG‐QBC939 cells transfected with TET1 gene or siRNA‐ TET1 . The results showed that compared with untreated cells, p‐gp expression remarkably decreased in cells with higher expression of TET1 and increased in cells with lower expression of TET1. The experiments were performed three times. (B) Nude mice were raised, divided equally and randomly into four groups, and subcutaneously inoculated with QBC939 and RG‐QBC939 in the backs. Two groups of mice were treated with 400 mg/kg gemcitabine at the first day when tumors reached a maximum size of 150 mm 3 and treated with 200 mg/kg gemcitabine at the eighth day and fifteenth day. The other two groups of mice were not treated with gemcitabine as control groups. Each mouse was weighed weekly, and mice were killed after 28 days (4 weeks) and necropsied. Tumor volume was monitored every week, and tumor weights were measured at the fourth week after mice were killed. (C) Tumors from the mice without treatment of chemotherapy had no significant differences in volume and weights between two groups. (D) After mice‐implanted CCA cells were treated with a conventional course of chemotherapy for 4 weeks, tumors, including the average tumor volume weekly and tumor weights derived from RG‐QBC939 cells, appeared larger than those in the other group. (E) Tumor tissues from QBC939 and RG‐QBC939 cells were immunohistochemically stained for Ki67. Ki67 expression was significantly higher in tumor tissues from mice with implanted RG‐QBC939 than that with implanted QBC939. Dots represent IHC score from 10 mice tumor tissues. The magnification is 200 times. (F) The expression of TET1 in tumors was immunohistochemically analyzed and the results showed that TET1 was expressed lowly in tumors derived from RG‐QBC939 cells. Dots represent IHC score from 10 mice tumor tissues. The magnification is 200 times. (G) Correlations between TET1 and P‐gp expression in cholangiocarcinoma tissues. The results suggested that expression of TET1 inversely correlated with P‐gp expression. The magnification is 200 times. The P ‐values represent the results of two‐tailed Student's t ‐test for two groups. Data were mean ±SD

    Article Snippet: After blocking, the sections were incubated with a rabbit monoclonal anti‐TET1 (#ab191698, Abcam, 1:300), anti‐P‐gp (#ab103477, Abcam, 1:50), or anti‐Ki67 (#ab15580, Abcam, 1:500) antibody diluted in PBS at 4°C overnight.

    Techniques: Expressing, Immunohistochemistry, Western Blot, Transfection, Mouse Assay, Derivative Assay, Staining, Two Tailed Test