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Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells
B cell-specific moloney murine leukemia virus integration site 1 (BMI1) is a transcriptional repressor of polycomb repressive complex 1, which is involved in the proliferation, senescence, migration, and tumorigenesis of cancer. Experimental researchers have convincingly linked BMI1 to tumorigenesis...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771375/ https://www.ncbi.nlm.nih.gov/pubmed/23820733 http://dx.doi.org/10.1007/s11010-013-1745-0 |
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author | Liang, Wu Zhu, Dingjun Cui, Xuejiang Su, Jiarui Liu, Hongwei Han, Jinli Zhao, Fengjin Xie, Wenlian |
author_facet | Liang, Wu Zhu, Dingjun Cui, Xuejiang Su, Jiarui Liu, Hongwei Han, Jinli Zhao, Fengjin Xie, Wenlian |
author_sort | Liang, Wu |
collection | PubMed |
description | B cell-specific moloney murine leukemia virus integration site 1 (BMI1) is a transcriptional repressor of polycomb repressive complex 1, which is involved in the proliferation, senescence, migration, and tumorigenesis of cancer. Experimental researchers have convincingly linked BMI1 to tumorigenesis. However, there is no study about the issue on the role of BMI1 in the proliferation, apoptosis, and migration of bladder cancer. To address this question, we examined the expression of BMI1 in bladder cancer tissues and used siRNA to knockdown BMI1 expression in bladder cancer T24 cells. Then we tested the cell proliferation by CCK8 assay and soft agar colony formation assay, apoptosis by flow cytometry assay, and cell invasiveness by transwell migration assay. Our results revealed that BMI1 promoted proliferation, migration, invasion, and progression in bladder cancer. Over-expression of BMI1 was correlated with tumor clinic-pathological features. BMI1 siRNA effectively inhibited bladder cancer cell proliferation and migration in vitro, and it promoted bladder cancer invasion, maybe by causing epithelial-to-mesenchymal transition. Our findings suggested that BMI1 may represent a novel diagnostic marker and a therapeutic target for bladder cancer, and deserves further investigation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11010-013-1745-0) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-3771375 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-37713752013-09-13 Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells Liang, Wu Zhu, Dingjun Cui, Xuejiang Su, Jiarui Liu, Hongwei Han, Jinli Zhao, Fengjin Xie, Wenlian Mol Cell Biochem Article B cell-specific moloney murine leukemia virus integration site 1 (BMI1) is a transcriptional repressor of polycomb repressive complex 1, which is involved in the proliferation, senescence, migration, and tumorigenesis of cancer. Experimental researchers have convincingly linked BMI1 to tumorigenesis. However, there is no study about the issue on the role of BMI1 in the proliferation, apoptosis, and migration of bladder cancer. To address this question, we examined the expression of BMI1 in bladder cancer tissues and used siRNA to knockdown BMI1 expression in bladder cancer T24 cells. Then we tested the cell proliferation by CCK8 assay and soft agar colony formation assay, apoptosis by flow cytometry assay, and cell invasiveness by transwell migration assay. Our results revealed that BMI1 promoted proliferation, migration, invasion, and progression in bladder cancer. Over-expression of BMI1 was correlated with tumor clinic-pathological features. BMI1 siRNA effectively inhibited bladder cancer cell proliferation and migration in vitro, and it promoted bladder cancer invasion, maybe by causing epithelial-to-mesenchymal transition. Our findings suggested that BMI1 may represent a novel diagnostic marker and a therapeutic target for bladder cancer, and deserves further investigation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11010-013-1745-0) contains supplementary material, which is available to authorized users. Springer US 2013-07-03 2013 /pmc/articles/PMC3771375/ /pubmed/23820733 http://dx.doi.org/10.1007/s11010-013-1745-0 Text en © The Author(s) 2013 https://creativecommons.org/licenses/by/2.0/ Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. |
spellingShingle | Article Liang, Wu Zhu, Dingjun Cui, Xuejiang Su, Jiarui Liu, Hongwei Han, Jinli Zhao, Fengjin Xie, Wenlian Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title | Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title_full | Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title_fullStr | Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title_full_unstemmed | Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title_short | Knockdown BMI1 expression inhibits proliferation and invasion in human bladder cancer T24 cells |
title_sort | knockdown bmi1 expression inhibits proliferation and invasion in human bladder cancer t24 cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771375/ https://www.ncbi.nlm.nih.gov/pubmed/23820733 http://dx.doi.org/10.1007/s11010-013-1745-0 |
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