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Id4 promotes cell proliferation in hepatocellular carcinoma
BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignant tumor in the world, especially in China. As a member of the inhibitor of differentiation (Id) family, Id4 has been reported to function in many cancer types, but relatively little is known about its role in HCC. The purpose of this stu...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5286768/ https://www.ncbi.nlm.nih.gov/pubmed/28143562 http://dx.doi.org/10.1186/s40880-017-0186-7 |
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author | Zhang, Yang Zhang, Li-Xing Liu, Xiao-Qin Zhao, Fang-Yu Ge, Chao Chen, Tao-Yang Yao, Ming Li, Jin-Jun |
author_facet | Zhang, Yang Zhang, Li-Xing Liu, Xiao-Qin Zhao, Fang-Yu Ge, Chao Chen, Tao-Yang Yao, Ming Li, Jin-Jun |
author_sort | Zhang, Yang |
collection | PubMed |
description | BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignant tumor in the world, especially in China. As a member of the inhibitor of differentiation (Id) family, Id4 has been reported to function in many cancer types, but relatively little is known about its role in HCC. The purpose of this study was to investigate the potential relationship between Id4 and HCC development and the underlying mechanism involving the function of Id4 in HCC. METHODS: We used quantitative real-time polymerase chain reaction and Western blotting to examine the RNA and protein expression of Id4. In addition, we used Cell Counting Kit-8 assay and colony formation assay to identify the function of Id4 in the regulation of cell proliferation in human HCC. RESULTS: We found that the expression of Id4 protein was up-regulated in tumor tissues from HCC patients. Overexpression of Id4 promoted HCC cell proliferation, clonogenicity in vitro, and tumorigenicity in vivo. Id4 knockdown experiments showed that silencing Id4 blocked the proliferation and colony formation ability of HCC cells in vitro. Furthermore, overexpression of CCAAT/enhancer-binding protein β inhibited Id4 expression in HCC cells. CONCLUSION: Id4 may be developed as a potent therapeutic agent for the treatment of HCC, but more details about the underlying mechanisms of action are needed. |
format | Online Article Text |
id | pubmed-5286768 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-52867682017-02-03 Id4 promotes cell proliferation in hepatocellular carcinoma Zhang, Yang Zhang, Li-Xing Liu, Xiao-Qin Zhao, Fang-Yu Ge, Chao Chen, Tao-Yang Yao, Ming Li, Jin-Jun Chin J Cancer Original Article BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignant tumor in the world, especially in China. As a member of the inhibitor of differentiation (Id) family, Id4 has been reported to function in many cancer types, but relatively little is known about its role in HCC. The purpose of this study was to investigate the potential relationship between Id4 and HCC development and the underlying mechanism involving the function of Id4 in HCC. METHODS: We used quantitative real-time polymerase chain reaction and Western blotting to examine the RNA and protein expression of Id4. In addition, we used Cell Counting Kit-8 assay and colony formation assay to identify the function of Id4 in the regulation of cell proliferation in human HCC. RESULTS: We found that the expression of Id4 protein was up-regulated in tumor tissues from HCC patients. Overexpression of Id4 promoted HCC cell proliferation, clonogenicity in vitro, and tumorigenicity in vivo. Id4 knockdown experiments showed that silencing Id4 blocked the proliferation and colony formation ability of HCC cells in vitro. Furthermore, overexpression of CCAAT/enhancer-binding protein β inhibited Id4 expression in HCC cells. CONCLUSION: Id4 may be developed as a potent therapeutic agent for the treatment of HCC, but more details about the underlying mechanisms of action are needed. BioMed Central 2017-02-01 /pmc/articles/PMC5286768/ /pubmed/28143562 http://dx.doi.org/10.1186/s40880-017-0186-7 Text en © The Author(s) 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Original Article Zhang, Yang Zhang, Li-Xing Liu, Xiao-Qin Zhao, Fang-Yu Ge, Chao Chen, Tao-Yang Yao, Ming Li, Jin-Jun Id4 promotes cell proliferation in hepatocellular carcinoma |
title | Id4 promotes cell proliferation in hepatocellular carcinoma |
title_full | Id4 promotes cell proliferation in hepatocellular carcinoma |
title_fullStr | Id4 promotes cell proliferation in hepatocellular carcinoma |
title_full_unstemmed | Id4 promotes cell proliferation in hepatocellular carcinoma |
title_short | Id4 promotes cell proliferation in hepatocellular carcinoma |
title_sort | id4 promotes cell proliferation in hepatocellular carcinoma |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5286768/ https://www.ncbi.nlm.nih.gov/pubmed/28143562 http://dx.doi.org/10.1186/s40880-017-0186-7 |
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