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MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large
Let-7 family members have been identified as tumor-suppressing microRNAs, which are important in human hepatocellular carcinoma (HCC). These family members may function differently as a result of different base sequences at the 3′end. The aim of this study was to determine the antitumor effects of m...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247110/ https://www.ncbi.nlm.nih.gov/pubmed/25435961 http://dx.doi.org/10.3892/ol.2014.2706 |
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author | WU, LINGJIAO WANG, QIANGFENG YAO, JIAN JIANG, HAN XIAO, CHENG WU, FUSHENG |
author_facet | WU, LINGJIAO WANG, QIANGFENG YAO, JIAN JIANG, HAN XIAO, CHENG WU, FUSHENG |
author_sort | WU, LINGJIAO |
collection | PubMed |
description | Let-7 family members have been identified as tumor-suppressing microRNAs, which are important in human hepatocellular carcinoma (HCC). These family members may function differently as a result of different base sequences at the 3′end. The aim of this study was to determine the antitumor effects of miR-let-7g/i (let-7g/i) on HCC cells and to investigate whether let-7g and let-7i have a combinatorial effect on HCC. The expression levels of let-7g/i in hepatoma cells were determined by quantitative reverse transcription polymerase chain reaction. In addition, a 5-ethynyl-2′-deoxyuridine retention assay and flow cytometry analysis were used to detect the effect of let-7g/i on the proliferation and apoptosis of BEL-7402 cells, respectively. The expression of anti-apoptotic protein B-cell lymphoma-extra large (Bcl-xL) was analyzed using western blot analysis. The results revealed that the expression levels of let-7g/i were significantly decreased in HCC cell lines when compared with L-02 cells. Furthermore, the overexpression of let-7g/i significantly suppressed DNA replication, inhibited cell proliferation and promoted apoptosis of BEL-7402 hepatoma cells. The expression of the anti-apoptotic protein, Bcl-xL, was inhibited by the combined role of let-7g and let-7i. We hypothesize that let-7g and let-7i exhibit a concurrent effect to regulate cell proliferation and the apoptosis of hepatoma cells, and this function is mediated by the Bcl-xL protein. |
format | Online Article Text |
id | pubmed-4247110 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-42471102014-11-28 MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large WU, LINGJIAO WANG, QIANGFENG YAO, JIAN JIANG, HAN XIAO, CHENG WU, FUSHENG Oncol Lett Articles Let-7 family members have been identified as tumor-suppressing microRNAs, which are important in human hepatocellular carcinoma (HCC). These family members may function differently as a result of different base sequences at the 3′end. The aim of this study was to determine the antitumor effects of miR-let-7g/i (let-7g/i) on HCC cells and to investigate whether let-7g and let-7i have a combinatorial effect on HCC. The expression levels of let-7g/i in hepatoma cells were determined by quantitative reverse transcription polymerase chain reaction. In addition, a 5-ethynyl-2′-deoxyuridine retention assay and flow cytometry analysis were used to detect the effect of let-7g/i on the proliferation and apoptosis of BEL-7402 cells, respectively. The expression of anti-apoptotic protein B-cell lymphoma-extra large (Bcl-xL) was analyzed using western blot analysis. The results revealed that the expression levels of let-7g/i were significantly decreased in HCC cell lines when compared with L-02 cells. Furthermore, the overexpression of let-7g/i significantly suppressed DNA replication, inhibited cell proliferation and promoted apoptosis of BEL-7402 hepatoma cells. The expression of the anti-apoptotic protein, Bcl-xL, was inhibited by the combined role of let-7g and let-7i. We hypothesize that let-7g and let-7i exhibit a concurrent effect to regulate cell proliferation and the apoptosis of hepatoma cells, and this function is mediated by the Bcl-xL protein. D.A. Spandidos 2015-01 2014-11-12 /pmc/articles/PMC4247110/ /pubmed/25435961 http://dx.doi.org/10.3892/ol.2014.2706 Text en Copyright © 2015, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles WU, LINGJIAO WANG, QIANGFENG YAO, JIAN JIANG, HAN XIAO, CHENG WU, FUSHENG MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title | MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title_full | MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title_fullStr | MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title_full_unstemmed | MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title_short | MicroRNA let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein B-cell lymphoma-extra large |
title_sort | microrna let-7g and let-7i inhibit hepatoma cell growth concurrently via downregulation of the anti-apoptotic protein b-cell lymphoma-extra large |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247110/ https://www.ncbi.nlm.nih.gov/pubmed/25435961 http://dx.doi.org/10.3892/ol.2014.2706 |
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