Research Papers:
UBE2T knockdown inhibits gastric cancer progression
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Abstract
Changjiang Luo1,*, Yunyi Yao2,*, Zeyuan Yu1, Huinian Zhou1, Lingyun Guo1, Junqiang Zhang1, Hongtai Cao1, Genyuan Zhang1, Yumin Li1, Zuoyi Jiao1
1Department of General Surgery, Lanzhou University Second Hospital and Key Laboratory of Digestive System Tumors of Gansu Province, Lanzhou, Gansu, 730030, China
2Department 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: [email protected]
Yumin Li, email: [email protected]
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.
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