UBE2T is upregulated, predicts poor prognosis, and promotes cell proliferation and invasion via inhibiting autophagy in ovarian cancer

Abstract

Background: Aberrant upregulation and oncogenic roles of UBE2T have been revealed in several cancers. However, the expression, clinical significance, and functions of UBE2T has not been explored in ovarian cancer (OC).Methods: In this study, the mRNA and protein expression of UBE2T in OC were detected via analyzing the online databases and immunohistochemical staining. Moreover, relations of UBE2T expression with clincopathological features and prognosis OC patients were further analyzed. Besides, the effects of UBE2T knockdown on growth, proliferation, and invasion of OC cells were investigated by CCK-8, plate clone formation, and Transwell assays. Finally, the underlying mechanism of UBE2T associated functions in OC was analyzed.Results: The results indicated that UBE2T was significantly upregulated in OC tissues. UBE2T expression was notably correlated with clinical features such as primary T stage, TNM stage in OC patients. UBE2T, acting as an independent prognostic indicator, was inversely associated with prognosis of OC patients. UBE2T knockdown remarkably suppressed the growth, proliferation, and invasion of OC cells indicating by impaired cell viability, less cell clones and invasive cells. Mechanistically, the oncogenic roles of UBE2T was exerted by inhibiting autophagy via maintaining AKT/mTOR activity in OC.Conclusion: Collectively, our findings confirm UBE2T upregulation predicts poor prognosis and promotes malignant progression via suppressing autophagy in OC, suggesting the promising values of UBE2T both in diagnosis and treatment of OC.