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Identification of hMex-3A and its effect on human bladder cancer cell proliferation
In this study, hMex-3A was selected from TCGA database as a research object to observe the effects of small interfering RNA (siRNA) targeting hMex-3A on the biological activities of human bladder cancer and explore its mechanism for the first time. In this study, there were 2 groups including negati...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617418/ https://www.ncbi.nlm.nih.gov/pubmed/28977858 http://dx.doi.org/10.18632/oncotarget.18050 |
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author | Huang, Ying Fang, Chao Shi, Jing-Wen Wen, Yu Liu, Da |
author_facet | Huang, Ying Fang, Chao Shi, Jing-Wen Wen, Yu Liu, Da |
author_sort | Huang, Ying |
collection | PubMed |
description | In this study, hMex-3A was selected from TCGA database as a research object to observe the effects of small interfering RNA (siRNA) targeting hMex-3A on the biological activities of human bladder cancer and explore its mechanism for the first time. In this study, there were 2 groups including negative control group and hMex-3A-siRNA-transfected cells group for 5637 and T24 cell lines, respectively. After bladder cancer cells were transfected with the interference RNA sequence, proliferation of transfected cells were assessed by Celigo Cell Counting, and apoptosis were detected by flow cytometry. The knockdown rate of hMex-3A was 74% in 5637 cells and 68% in T24 cells after RNA interference. In addition, Celigo Cell Counting indicated that cell viability was significantly lower in hMex-3A-siRNA-transfected cells group (2196/well) than in negative control group (6777/well) (P < 0.05), but T24 cells did not show statistical significance between hMex-3A-siRNA-transfected cells group (5799/well) and negative control group (7899/well) (P >0.05). Flow cytometer showed that apoptosis was the highest and cells were significantly blocked after cells were transfected in hMex-3A-siRNA-transfected cells group in 5 days later (P < 0.05). Mex-3A protein was detected in bladder carcinoma sections with a mean staining intensity of 7.06±2.60. Mex-3A protein expression was significantly higher in cancerous tissue than in para-cancerous tissue (P <0.05). Our study suggested that siRNA targeting hMex-3A could markedly inhibit cell proliferation and promote apoptosis in 5637 cells. These might have significant implications to bladder carcinogenesis and serve as a potential target for the treatment of bladder cancer. |
format | Online Article Text |
id | pubmed-5617418 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-56174182017-10-03 Identification of hMex-3A and its effect on human bladder cancer cell proliferation Huang, Ying Fang, Chao Shi, Jing-Wen Wen, Yu Liu, Da Oncotarget Research Paper In this study, hMex-3A was selected from TCGA database as a research object to observe the effects of small interfering RNA (siRNA) targeting hMex-3A on the biological activities of human bladder cancer and explore its mechanism for the first time. In this study, there were 2 groups including negative control group and hMex-3A-siRNA-transfected cells group for 5637 and T24 cell lines, respectively. After bladder cancer cells were transfected with the interference RNA sequence, proliferation of transfected cells were assessed by Celigo Cell Counting, and apoptosis were detected by flow cytometry. The knockdown rate of hMex-3A was 74% in 5637 cells and 68% in T24 cells after RNA interference. In addition, Celigo Cell Counting indicated that cell viability was significantly lower in hMex-3A-siRNA-transfected cells group (2196/well) than in negative control group (6777/well) (P < 0.05), but T24 cells did not show statistical significance between hMex-3A-siRNA-transfected cells group (5799/well) and negative control group (7899/well) (P >0.05). Flow cytometer showed that apoptosis was the highest and cells were significantly blocked after cells were transfected in hMex-3A-siRNA-transfected cells group in 5 days later (P < 0.05). Mex-3A protein was detected in bladder carcinoma sections with a mean staining intensity of 7.06±2.60. Mex-3A protein expression was significantly higher in cancerous tissue than in para-cancerous tissue (P <0.05). Our study suggested that siRNA targeting hMex-3A could markedly inhibit cell proliferation and promote apoptosis in 5637 cells. These might have significant implications to bladder carcinogenesis and serve as a potential target for the treatment of bladder cancer. Impact Journals LLC 2017-05-22 /pmc/articles/PMC5617418/ /pubmed/28977858 http://dx.doi.org/10.18632/oncotarget.18050 Text en Copyright: © 2017 Huang et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Huang, Ying Fang, Chao Shi, Jing-Wen Wen, Yu Liu, Da Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title | Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title_full | Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title_fullStr | Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title_full_unstemmed | Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title_short | Identification of hMex-3A and its effect on human bladder cancer cell proliferation |
title_sort | identification of hmex-3a and its effect on human bladder cancer cell proliferation |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5617418/ https://www.ncbi.nlm.nih.gov/pubmed/28977858 http://dx.doi.org/10.18632/oncotarget.18050 |
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