Abstract
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.
Highlights
Esophageal cancer (EC) is one of the leading causes of cancer related death in the world and there are about 400,200 people died from EC in 2012 [1]
regulator of Cullins-1 (ROC1) was reported to be overexpressed in a number of cancers [8,9,10,11], which was associated with poor prognosis of several cancers, such as non-muscle-invasive bladder transitional cell carcinoma (NMIBC) [9], gastric cancer [8, 10] and liver cancer [12]
Statistical analysis demonstrated that ROC1 was overexpressed in Esophageal squamous cell carcinoma (ESCC) tissues compared with their corresponding adjacent normal tissues (Figure 1B), which was confirmed by Western blotting analysis (Figure 1D)
Summary
Esophageal cancer (EC) is one of the leading causes of cancer related death in the world and there are about 400,200 people died from EC in 2012 [1]. Esophageal squamous cell carcinoma (ESCC) is a major histological subtype among all types of the esophageal tumors, especially in China [2]. ROC1 was reported to be overexpressed in a number of cancers [8,9,10,11], which was associated with poor prognosis of several cancers, such as non-muscle-invasive bladder transitional cell carcinoma (NMIBC) [9], gastric cancer [8, 10] and liver cancer [12]. Dysfunction of ROC1 induced embryonic death and abnormal meiosis [13]. These reports suggested that ROC1 could act as an attractive anticancer target. There is little known about the expression and role of ROC1 in esophageal cancer
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