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Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma
BACKGROUND: Bladder urothelial carcinoma is the most common genitourinary system cancer in China. The objective of this study was to investigate whether the miR-9 can regulate the invasion ability of human bladder transitional cell carcinoma cells by down-regulation of CBX7. MATERIAL/METHODS: The ex...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307688/ https://www.ncbi.nlm.nih.gov/pubmed/25596753 http://dx.doi.org/10.12659/MSM.893232 |
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author | Xie, Dalong Shang, Chao Zhang, Hui Guo, Yan Tong, Xiaojie |
author_facet | Xie, Dalong Shang, Chao Zhang, Hui Guo, Yan Tong, Xiaojie |
author_sort | Xie, Dalong |
collection | PubMed |
description | BACKGROUND: Bladder urothelial carcinoma is the most common genitourinary system cancer in China. The objective of this study was to investigate whether the miR-9 can regulate the invasion ability of human bladder transitional cell carcinoma cells by down-regulation of CBX7. MATERIAL/METHODS: The expression of miR-9 was detected by quantitative real-time PCR in bladder transitional cell carcinomas (TCC) and normal bladder transitional cell (NBTC) samples. Bioinformatics software was used to predict some potential target genes of miR-9. T24 cells were transfected with pre-miR-9, and the CBX7 protein expression was detected by Western blot. Luciferase activities assay was selected to verify that CBX7 was a direct and specific gene of miR-9. T24 cells were transfected with pcDNA-CBX7, and the expression of CBX7 gene was detected. Then, the transwell assay was used to detect the invasion ability of T24 cells with CBX7 over-expression. RESULTS: The expression of miR-9 increased significantly in human TCC specimens compared to that in NBTC specimens. TargetScan and PicTar software programs predicted CBX7 gene was a target gene of miR-9. The pre-miR-9 could up-regulate the miR-9 expression and down-regulate CBX7 protein expression. The luciferase activities assay verified that CBX7 gene was a direct and specific target gene of miR-9. The pcDNA-CBX7 transfection could up-regulate the CBX7 protein expression, and the invasion ability of T24 cells with CBX7 over-expression decreased significantly. CONCLUSIONS: Aberrantly expressed miR-9 contributes to T24 cells invasion, partly through directly down-regulating CBX7 protein expression in TCC. This miRNA signature offers a new potential therapeutic target for TCC. |
format | Online Article Text |
id | pubmed-4307688 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-43076882015-01-27 Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma Xie, Dalong Shang, Chao Zhang, Hui Guo, Yan Tong, Xiaojie Med Sci Monit Molecular Biology BACKGROUND: Bladder urothelial carcinoma is the most common genitourinary system cancer in China. The objective of this study was to investigate whether the miR-9 can regulate the invasion ability of human bladder transitional cell carcinoma cells by down-regulation of CBX7. MATERIAL/METHODS: The expression of miR-9 was detected by quantitative real-time PCR in bladder transitional cell carcinomas (TCC) and normal bladder transitional cell (NBTC) samples. Bioinformatics software was used to predict some potential target genes of miR-9. T24 cells were transfected with pre-miR-9, and the CBX7 protein expression was detected by Western blot. Luciferase activities assay was selected to verify that CBX7 was a direct and specific gene of miR-9. T24 cells were transfected with pcDNA-CBX7, and the expression of CBX7 gene was detected. Then, the transwell assay was used to detect the invasion ability of T24 cells with CBX7 over-expression. RESULTS: The expression of miR-9 increased significantly in human TCC specimens compared to that in NBTC specimens. TargetScan and PicTar software programs predicted CBX7 gene was a target gene of miR-9. The pre-miR-9 could up-regulate the miR-9 expression and down-regulate CBX7 protein expression. The luciferase activities assay verified that CBX7 gene was a direct and specific target gene of miR-9. The pcDNA-CBX7 transfection could up-regulate the CBX7 protein expression, and the invasion ability of T24 cells with CBX7 over-expression decreased significantly. CONCLUSIONS: Aberrantly expressed miR-9 contributes to T24 cells invasion, partly through directly down-regulating CBX7 protein expression in TCC. This miRNA signature offers a new potential therapeutic target for TCC. International Scientific Literature, Inc. 2015-01-18 /pmc/articles/PMC4307688/ /pubmed/25596753 http://dx.doi.org/10.12659/MSM.893232 Text en © Med Sci Monit, 2015 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Molecular Biology Xie, Dalong Shang, Chao Zhang, Hui Guo, Yan Tong, Xiaojie Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title | Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title_full | Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title_fullStr | Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title_full_unstemmed | Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title_short | Up-Regulation of miR-9 Target CBX7 to Regulate Invasion Ability of Bladder Transitional Cell Carcinoma |
title_sort | up-regulation of mir-9 target cbx7 to regulate invasion ability of bladder transitional cell carcinoma |
topic | Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4307688/ https://www.ncbi.nlm.nih.gov/pubmed/25596753 http://dx.doi.org/10.12659/MSM.893232 |
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