ROCK2 promotes HCC proliferation by CEBPD inhibition through phospho-GSK3β/β-catenin signaling
ROCK2 promotes HCC proliferation by CEBPD inhibition through phospho-GSK3β/β-catenin signaling
复制标题
ROCK2 通过磷酸化 GSK3 β/β-连环蛋白信号传导抑制 CEBPD 促进 HCC 增殖
DOI：
10.1016/j.febslet.2015.03.004
复制
发表时间：
2015-04-13
期刊：
影响因子：
3.5
通讯作者：
Shao, Jianghua
中科院分区：
文献类型：
--
作者：
Li, Ming;Zhou, Wei;Shao, Jianghua
Rho相关激酶2（Rock 2）被认为促进肝细胞癌（HCC）的肿瘤发生。CCAAT/增强子结合蛋白δ（CEBPD）作为肿瘤抑制因子发挥作用。在本研究中，我们发现Rock 2和CEBPD的表达呈负相关。Rock 2的敲低增加了CEBPD的表达，并在体外和体内抑制肝癌细胞的增殖。从机制上讲，我们发现Rock 2通过p-GSK 3 β/β-连环蛋白途径调节CEBPD表达。综上所述，我们确定了一种新的Rock 2-p-GSK 3 β/β-catenin-CEBPD调节回路，其功能障碍可能有助于HCC的致瘤特征。(C)2015年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
Rho-associated kinase 2 (Rock2) is known to promote tumorigenesis in hepatocellular carcinoma (HCC). CCAAT/enhancer-binding protein delta (CEBPD) functions as a tumor suppressor. In this study, we found that the expression of Rock2 and CEBPD are inversely correlated. Knockdown of Rock2 increased CEBPD expression and inhibited the proliferation of HCC cells in vitro and in vivo. Mechanistically, we found that Rock2 regulates CEBPD expression through the p-GSK3 beta/beta-catenin pathway. Taken together, we identified a novel Rock2-p-GSK3 beta/beta-catenin-CEBPD regulatory circuitry, the dysfunction of which may contribute to the tumorigenic characteristic of HCC. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.