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Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions
Ring finger protein 187 (RNF187) has been identified to be a co-activator linking c Jun to Ras signaling. However, the expression and function of RNF187 in hepatocellular carcinomas (HCC) remains unclear. Here, we tried to determine the expression and roles of RNF187 in hepatocellular carcinomas (HC...
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/PMC5731920/ https://www.ncbi.nlm.nih.gov/pubmed/29254210 http://dx.doi.org/10.18632/oncotarget.22056 |
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author | Yu, Song-Lin Wu, Jin-Cai Liu, Peng-Fei Liu, Kai Ye, Chun Zhou, Kai-Lun Li, Zhuo-Ri Xu, Ya-Ping |
author_facet | Yu, Song-Lin Wu, Jin-Cai Liu, Peng-Fei Liu, Kai Ye, Chun Zhou, Kai-Lun Li, Zhuo-Ri Xu, Ya-Ping |
author_sort | Yu, Song-Lin |
collection | PubMed |
description | Ring finger protein 187 (RNF187) has been identified to be a co-activator linking c Jun to Ras signaling. However, the expression and function of RNF187 in hepatocellular carcinomas (HCC) remains unclear. Here, we tried to determine the expression and roles of RNF187 in hepatocellular carcinomas (HCC).The expression of RNF187 was determined in HCC tissues and cell lines, and we found that RNF187 expressed highly in HCC tissues compared with the corresponding adjacent liver tissues both in mRNA and protein level, which was consistent with the result of immunohistochemistry on HCC tissue microarrays. In HCC cell lines, the level of RNF187 was positively associated with the HCC cells metastatic potential. By the RNF187 interference and cDNA transfection, we showed that the high level of RNF187 induced the HCC cells invasion and metastasis both in vitro and in vivo, as well as the high ability of colony formation.Mechanistically, we detected the high level of RNF187 promoted cell scatter by inducing epithelial-mesenchymal transition (EMT). Clinically, the high level of RNA187 was significantly correlated with a malignant phenotype, including larger tumor size, multiple tumors, and microvascular invasion. Importantly, high level of RNF187 correlated with HCC patients' shorter OS and lower disease free survival rates than those with low level of RNF187. Our results revealed that elevated expression of RNF187 induced hepatocellular carcinoma cell epithelial to mesenchymal transitions, and represented a novel marker for predicting the poor prognosis of HCC. |
format | Online Article Text |
id | pubmed-5731920 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-57319202017-12-17 Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions Yu, Song-Lin Wu, Jin-Cai Liu, Peng-Fei Liu, Kai Ye, Chun Zhou, Kai-Lun Li, Zhuo-Ri Xu, Ya-Ping Oncotarget Research Paper Ring finger protein 187 (RNF187) has been identified to be a co-activator linking c Jun to Ras signaling. However, the expression and function of RNF187 in hepatocellular carcinomas (HCC) remains unclear. Here, we tried to determine the expression and roles of RNF187 in hepatocellular carcinomas (HCC).The expression of RNF187 was determined in HCC tissues and cell lines, and we found that RNF187 expressed highly in HCC tissues compared with the corresponding adjacent liver tissues both in mRNA and protein level, which was consistent with the result of immunohistochemistry on HCC tissue microarrays. In HCC cell lines, the level of RNF187 was positively associated with the HCC cells metastatic potential. By the RNF187 interference and cDNA transfection, we showed that the high level of RNF187 induced the HCC cells invasion and metastasis both in vitro and in vivo, as well as the high ability of colony formation.Mechanistically, we detected the high level of RNF187 promoted cell scatter by inducing epithelial-mesenchymal transition (EMT). Clinically, the high level of RNA187 was significantly correlated with a malignant phenotype, including larger tumor size, multiple tumors, and microvascular invasion. Importantly, high level of RNF187 correlated with HCC patients' shorter OS and lower disease free survival rates than those with low level of RNF187. Our results revealed that elevated expression of RNF187 induced hepatocellular carcinoma cell epithelial to mesenchymal transitions, and represented a novel marker for predicting the poor prognosis of HCC. Impact Journals LLC 2017-10-19 /pmc/articles/PMC5731920/ /pubmed/29254210 http://dx.doi.org/10.18632/oncotarget.22056 Text en Copyright: © 2017 Yu 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 3.0 (http://creativecommons.org/licenses/by/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 Yu, Song-Lin Wu, Jin-Cai Liu, Peng-Fei Liu, Kai Ye, Chun Zhou, Kai-Lun Li, Zhuo-Ri Xu, Ya-Ping Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title | Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title_full | Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title_fullStr | Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title_full_unstemmed | Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title_short | Up-regulation of RNF187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
title_sort | up-regulation of rnf187 induces hepatocellular carcinoma cell epithelial to mesenchymal transitions |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5731920/ https://www.ncbi.nlm.nih.gov/pubmed/29254210 http://dx.doi.org/10.18632/oncotarget.22056 |
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