期刊
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 55, 期 4, 页码 661-671出版社
SCIENCE PRESS
DOI: 10.3724/abbs.2023076
关键词
hepatocellular carcinoma; epithelial-mesenchymal transition; RNF8; drug resistance
In this study, the expression of RNF8 was found to be up-regulated in HCC tissues and positively correlated with poor prognosis of HCC. Silencing RNF8 attenuated the migration of HCC cells and inhibited EMT by regulating the expressions of specific proteins. High RNF8 expression predicted poor survival benefits from sorafenib, and RNF8 depletion enhanced the sensitivity of HCC cells to sorafenib and lenvatinib treatment.
Despite substantial advances that have been made in understanding the etiology of hepatocellular carcinoma (HCC), the early-stage diagnosis and treatment of advanced-stage HCC remain a major challenge. RNF8, an E3 ligase important for the DNA damage response, has been proven to facilitate the progression of breast and lung cancer, but its role in HCC remains unclear. In this study, we find that the expression of RNF8 is up-regulated in HCC tissues and positively correlated with poor prognosis of HCC. Furthermore, silencing RNF8 by siRNAs attenuates the migration of HCC cells and inhibits epithelial-mesenchymal transition (EMT) by regulating the expressions of proteins including N-cadherin, beta-catenin, snail, and ZO-1. Moreover, Kaplan.Meier survival analysis shows that high RNF8 expression predicts poor survival benefits from sorafenib. Finally, cell viability assay demonstrates that RNF8 depletion enhances the sensitivity of HCC cells to sorafenib and lenvatinib treatment. We hypothesize that the inhibitory role of RNF8 in EMT and its enhancing effects on anti-cancer drugs orchestrate the protective effects of RNF8 deficiency in HCC, which indicates its potential in clinical application.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据