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Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells
In recent years it was found that the synthesis and biological activity of ribosomes are closely associated with tumor cell growth, tumorigenesis, and malignant transformation. However, the role of regulator of ribosome synthesis 1 (RRS1) in hepatocellular carcinoma (HCC) has not yet been reported....
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652961/ https://www.ncbi.nlm.nih.gov/pubmed/28849112 http://dx.doi.org/10.3892/or.2017.5906 |
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author | Wang, Jitao Li, Zhi Zuo, Changzeng Xie, Qingfan Li, Hui Jia, Junhong Zhen, Zhongguang Qi, Ruizhao Li, Zhiwei Liu, Dengxiang Sun, Baijun |
author_facet | Wang, Jitao Li, Zhi Zuo, Changzeng Xie, Qingfan Li, Hui Jia, Junhong Zhen, Zhongguang Qi, Ruizhao Li, Zhiwei Liu, Dengxiang Sun, Baijun |
author_sort | Wang, Jitao |
collection | PubMed |
description | In recent years it was found that the synthesis and biological activity of ribosomes are closely associated with tumor cell growth, tumorigenesis, and malignant transformation. However, the role of regulator of ribosome synthesis 1 (RRS1) in hepatocellular carcinoma (HCC) has not yet been reported. In the present study, we aimed to examine the potential role of RRS1 in tumor cell growth by using a lentivirus-mediated RNA interference (RNAi) system in the HCC cell line SMMC-7721 in vitro. Compared with that of the negative control group (Lv-shCon), the mRNA and protein expression levels of RRS1 in SMMC-7721 cells transfected with Lv-shRRS1 were significantly decreased. Further experiments found that silencing of RRS1 gene expression in SMMC-7721 cells significantly suppressed cell proliferation, inhibited colony formation capacity, increased apoptosis and arrested cells in the G1 phase. These results suggest that the RRS1 gene plays a critical role in cell proliferation, colony formation, cell apoptosis and cell cycle distribution in human HCC cells, and that silencing of RRS1 by RNAi is a promising therapeutic approach for the treatment of HCC, and should be further developed. |
format | Online Article Text |
id | pubmed-5652961 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56529612017-11-02 Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells Wang, Jitao Li, Zhi Zuo, Changzeng Xie, Qingfan Li, Hui Jia, Junhong Zhen, Zhongguang Qi, Ruizhao Li, Zhiwei Liu, Dengxiang Sun, Baijun Oncol Rep Articles In recent years it was found that the synthesis and biological activity of ribosomes are closely associated with tumor cell growth, tumorigenesis, and malignant transformation. However, the role of regulator of ribosome synthesis 1 (RRS1) in hepatocellular carcinoma (HCC) has not yet been reported. In the present study, we aimed to examine the potential role of RRS1 in tumor cell growth by using a lentivirus-mediated RNA interference (RNAi) system in the HCC cell line SMMC-7721 in vitro. Compared with that of the negative control group (Lv-shCon), the mRNA and protein expression levels of RRS1 in SMMC-7721 cells transfected with Lv-shRRS1 were significantly decreased. Further experiments found that silencing of RRS1 gene expression in SMMC-7721 cells significantly suppressed cell proliferation, inhibited colony formation capacity, increased apoptosis and arrested cells in the G1 phase. These results suggest that the RRS1 gene plays a critical role in cell proliferation, colony formation, cell apoptosis and cell cycle distribution in human HCC cells, and that silencing of RRS1 by RNAi is a promising therapeutic approach for the treatment of HCC, and should be further developed. D.A. Spandidos 2017-10 2017-08-14 /pmc/articles/PMC5652961/ /pubmed/28849112 http://dx.doi.org/10.3892/or.2017.5906 Text en Copyright: © Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Wang, Jitao Li, Zhi Zuo, Changzeng Xie, Qingfan Li, Hui Jia, Junhong Zhen, Zhongguang Qi, Ruizhao Li, Zhiwei Liu, Dengxiang Sun, Baijun Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title | Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title_full | Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title_fullStr | Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title_full_unstemmed | Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title_short | Knockdown of RRS1 by lentiviral-mediated RNAi promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
title_sort | knockdown of rrs1 by lentiviral-mediated rnai promotes apoptosis and suppresses proliferation of human hepatocellular carcinoma cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652961/ https://www.ncbi.nlm.nih.gov/pubmed/28849112 http://dx.doi.org/10.3892/or.2017.5906 |
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