Targeting the overexpressed ROC1 induces G2 cell cycle arrest and apoptosis in esophageal cancer cells
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Jingyang Zhang1,*, Shuo Li1,*, Zhaoyang Shang1, Shan Lin1, Peng Gao1, Yi Zhang1, Shuaiheng Hou1, Saijun Mo1, Wenbo Cao1, Ziming Dong1, Tao Hu1, Ping Chen1
1College of Basic Medical Sciences, Zhengzhou University, Collaborative Innovation Center of Henan Province for Cancer Chemoprevention, Zhengzhou, 450001, China
*Jingyang Zhang and Shuo Li contributed to this work equally
Ping Chen, email: email@example.com
Tao Hu, email: firstname.lastname@example.org
Keywords: ROC1, cell cycle, apoptosis, esophageal cancer, NOXA
Received: June 21, 2016 Accepted: February 20, 2017 Published: March 16, 2017
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.
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