胶质瘤是一种中枢神经系统（CNS）恶性肿瘤，具有较高的异质性和死亡率，严重威胁患者的健康。神经胶质瘤患者的总生存期相对较短，确定新的分子靶点对于制定有效的治疗策略至关重要。 UBE2K 是一种泛素结合酶，在多种恶性肿瘤中具有致癌功能。然而，UBE2K 是否参与神经胶质瘤仍不清楚。在此，在神经胶质瘤细胞中，发现UBE2K在U87和U251细胞中高表达。随后用si-UBE2K转染U87和U251细胞以沉默UBE2K，以si-NC转染作为阴性对照。在U87和U251细胞中，转染si-UBE2K 48和72小时后，细胞活力急剧降低。 si-UBE2K转染的U87和U251细胞中集落数量明显减少，迁移细胞和侵袭细胞数量减少，相对伤口愈合率下降。此外，转染si-UBE2K后，U87和U251细胞中Bcl-2水平显着降低，而Bax和cleaved-caspase-3水平急剧升高。此外，通过si-UBE2K转染，U87和U251细胞中p62水平显着下降，而Beclin-1和LC-3 II/I水平大大增加。此外，si-UBE2K对U87和U251细胞凋亡和自噬的促进作用被自噬抑制剂3-MA的共培养消除。总的来说，UBE2K 可能通过抑制自噬相关的细胞凋亡来促进神经胶质瘤细胞的体外生长，这可能是治疗神经胶质瘤的一个有希望的靶标。© 2024 作者。 《生物化学和分子毒理学杂志》由 Wiley periodicals LLC 出版。

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.© 2024 The Author(s). Journal of Biochemical and Molecular Toxicology published by Wiley Periodicals LLC.