Silencing UBE2K inhibits the growth of glioma cells by inducing the autophagy‐related apoptosis

Glioma is a central nervous system (CNS) malignant tumor with high heterogeneity and mortality, which severely threatens the health of patients. The overall survival of glioma patients is relatively short and it is critical to identify new molecular targets for developing effective treatment strategies. UBE2K is a ubiquitin conjugating enzyme with oncogenic function in several malignant tumors. However, whether UBE2K participates in gliomas remains unknown. Herein, in glioma cells, UBE2K was found highly expressed in U87 and U251 cells. Subsequently, U87 and U251 cells were transfected with si‐UBE2K to silence UBE2K, with the si‐NC transfection as the negative control. In both U87 and U251 cells, the cell viability was sharply reduced by transfecting si‐UBE2K for 48 and 72 h. Markedly decreased colony number, reduced number of migrated cells and invaded cells, and declined relative wound healing rate were observed in si‐UBE2K transfected U87 and U251 cells. Moreover, the Bcl‐2 level was markedly reduced, while the Bax and cleaved‐caspase‐3 levels were sharply increased in U87 and U251 cells after the si‐UBE2K transfection. Furthermore, the p62 level was signally declined, while the Beclin‐1 and LC‐3 II/I levels were greatly increased in U87 and U251 cells by the si‐UBE2K transfection. Furthermore, the facilitating effect of si‐UBE2K on the apoptosis and autophagy in U87 and U251 cells was abolished by the coculture of 3‐MA, an inhibitor of autophagy. Collectively, UBE2K facilitated the in vitro growth of glioma cells, possibly by inhibiting the autophagy‐related apoptosis, which might be a promising target for treating glioma. UBE2K facilitated the in vitro growth of glioma cells, possibly by inhibiting the autophagy‐related apoptosis, which might be a promising target for treating glioma.