The Suppressive Role of SOX7 in Hepatocarcinogenesis
SOX7 is a transcription factor mediating various developmental processes. However, its role in hepatocellular carcinoma (HCC) remains unclear. Here, we assessed the role of SOX7 in hepatocarcinogenesis. We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor sa...
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pubmed-40163112014-05-14 The Suppressive Role of SOX7 in Hepatocarcinogenesis Wang, Chong Guo, Yu Wang, Jing Min, Zhiqun Research Article SOX7 is a transcription factor mediating various developmental processes. However, its role in hepatocellular carcinoma (HCC) remains unclear. Here, we assessed the role of SOX7 in hepatocarcinogenesis. We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size. SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7). Overexpression of SOX7 could inhibit HCC cell growth, with G1to S phase arrest. In SOX7-overexpression cells, cyclin D1 and c-myc, two cell cycle promoters, were down-regulated. Moreover, ectopic expression of cyclin D1 or c-myc could override G1 to S pahse arrest induced by SOX7. Furthermore, overexpression of SOX7 suppressed tumor formation with down-regulation of cyclin D1 and c-myc in vivo. The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors. Taken together, our study suggests that SOX7 plays an important inhibitory role in hepatocarcinogenesis, and might be a novel target for HCC therapy. Public Library of Science 2014-05-09 /pmc/articles/PMC4016311/ /pubmed/24816720 http://dx.doi.org/10.1371/journal.pone.0097433 Text en © 2014 Wang et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Wang, Chong Guo, Yu Wang, Jing Min, Zhiqun |
spellingShingle |
Wang, Chong Guo, Yu Wang, Jing Min, Zhiqun The Suppressive Role of SOX7 in Hepatocarcinogenesis |
author_facet |
Wang, Chong Guo, Yu Wang, Jing Min, Zhiqun |
author_sort |
Wang, Chong |
title |
The Suppressive Role of SOX7 in Hepatocarcinogenesis |
title_short |
The Suppressive Role of SOX7 in Hepatocarcinogenesis |
title_full |
The Suppressive Role of SOX7 in Hepatocarcinogenesis |
title_fullStr |
The Suppressive Role of SOX7 in Hepatocarcinogenesis |
title_full_unstemmed |
The Suppressive Role of SOX7 in Hepatocarcinogenesis |
title_sort |
suppressive role of sox7 in hepatocarcinogenesis |
description |
SOX7 is a transcription factor mediating various developmental processes. However, its role in hepatocellular carcinoma (HCC) remains unclear. Here, we assessed the role of SOX7 in hepatocarcinogenesis. We found HCC samples exhibited lower levels of SOX7 mRNA and protein expression than non-tumor samples, and the expression of SOX7 was negatively correlated with tumor size. SOX7 expression was also reduced in four HCC cell lines (SMMC-7721, Hep3B, HepG2 and Huh 7). Overexpression of SOX7 could inhibit HCC cell growth, with G1to S phase arrest. In SOX7-overexpression cells, cyclin D1 and c-myc, two cell cycle promoters, were down-regulated. Moreover, ectopic expression of cyclin D1 or c-myc could override G1 to S pahse arrest induced by SOX7. Furthermore, overexpression of SOX7 suppressed tumor formation with down-regulation of cyclin D1 and c-myc in vivo. The expression of Ki-67, a proliferation marker, was also reduced in SOX7-overexpression tumors. Taken together, our study suggests that SOX7 plays an important inhibitory role in hepatocarcinogenesis, and might be a novel target for HCC therapy. |
publisher |
Public Library of Science |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4016311/ |
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1612087513325764608 |