Targeting the overexpressed ROC1 induces G2 cell cycle arrest and apoptosis in esophageal cancer cells.
Targeting the overexpressed ROC1 induces G2 cell cycle arrest and apoptosis in esophageal cancer cells.
复制标题
靶向过度表达的 ROC1 诱导食管癌细胞 G2 细胞周期停滞和凋亡
DOI：
10.18632/oncotarget.16250
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发表时间：
2017-04-25
期刊：
影响因子：
--
通讯作者：
Chen P
中科院分区：
文献类型：
--
作者：
Zhang J;Li S;Shang Z;Lin S;Gao P;Zhang Y;Hou S;Mo S;Cao W;Dong Z;Hu T;Chen P
Recent reports showed that regulator of Cullins-1 (ROC1) play an important role in tumor progression in a tumor-specific manner. However, the role and mechanism of ROC1 in esophageal cancer remains elusive. Here we demonstrated that ROC1 was overexpressed in esophageal squamous cell carcinomas, which was positive associated with poor prognosis of esophageal cancer patients. ROC1 knockdown significantly inhibited the growth of esophageal cancer cells in vitro and in vivo. Mechanistically, ROC1 silencing induced G2 cell cycle arrest and triggered apoptosis by accumulating the pro-apoptotic protein NOXA. Consistently, the downregulation of NOXA expression via siRNA substantially attenuated apoptosis induced by ROC1 silencing. These findings suggest that ROC1 is an appealing drug target for esophageal cancer.
