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Silencing UBE2K inhibits the growth of glioma cells by inducing the autophagy-related apoptosis.
Xin, Zhen; Holgersson, Kristian; Zhu, Pengcheng; Tan, Hongtu; Shi, Guangyan; Szekely, Laszlo; Wu, Tao.
Afiliación
  • Xin Z; Medical Laboratory center, The Second Hospital of Shandong University, Jinan, China.
  • Holgersson K; Loma Linda University, Loma Linda, California, USA.
  • Zhu P; Interventional department of Encephalopathy, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
  • Tan H; Interventional department of Encephalopathy, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
  • Shi G; Medical Laboratory center, The Second Hospital of Shandong University, Jinan, China.
  • Szekely L; Department of Pathology/Cytology, Karolinska University Laboratory, Stockholm, Sweden.
  • Wu T; Interventional department of Encephalopathy, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
J Biochem Mol Toxicol ; 38(7): e23758, 2024 Jul.
Article en En | MEDLINE | ID: mdl-38963134
ABSTRACT
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autofagia / Apoptosis / Enzimas Ubiquitina-Conjugadoras / Glioma Límite: Humans Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Autofagia / Apoptosis / Enzimas Ubiquitina-Conjugadoras / Glioma Límite: Humans Idioma: En Revista: J Biochem Mol Toxicol Asunto de la revista: BIOLOGIA MOLECULAR / BIOQUIMICA / TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos