UBE2T knockdown inhibits gastric cancer progression

// Changjiang Luo 1, * , Yunyi Yao 2, * , Zeyuan Yu 1 , Huinian Zhou 1 , Lingyun Guo 1 , Junqiang Zhang 1 , Hongtai Cao 1 , Genyuan Zhang 1 , Yumin Li 1 , Zuoyi Jiao 1 1 Department of General Surgery, Lanzhou University Second Hospital and Key Laboratory of Digestive System Tumors of Gansu Province, Lanzhou, Gansu, 730030, China 2 Department of Medical Technology and Key Laboratory of Biotechnology for Laboratory Medicine of Suzhou, Suzhou Vocational Health College, Suzhou, Jiangsu, 215009, China * These authors contributed equally to this work Correspondence to: Zuoyi Jiao, email: jiaozy@lzu.edu.cn Yumin Li, email: liym@lzu.edu.cn Keywords: UBE2T, ubiquitination, gastric cancer, tumor apoptosis, invasion and metastasis Received: October 28, 2016      Accepted: February 22, 2017      Published: March 06, 2017 ABSTRACT Ubiquitin-conjugating enzymes (E2 enzymes) such as UBE2T target proteins for degradation via the proteasome. Here, we examined the effects of UBE2T on the progression of gastric cancer. UBE2T was highly expressed in gastric tumors and gastric cancer cells. siRNA-mediated suppression of UBE2T inhibited gastric cancer cell proliferation and colony formation by promoting cell cycle arrest at G2/M phase and increasing apoptosis. Suppression of UBE2T also attenuated the invasive and metastatic abilities of gastric cancer cells by altering expression of epithelial-mesenchymal transition (EMT)-related factors. A xenograft model in which nude mice were injected with UBE2T knockdown human gastric cancer cells confirmed that suppression of UBE2T also decreased tumor formation and growth in vivo . Expression levels of CCND1, Phospho-GSK3B, WNT family members, and MYC were all affected by UBE2T knockdown. These results suggest that UBE2T plays a critical role in gastric cancer, and that it may serve as a useful prognostic biomarker and therapeutic target in gastric cancer patients.