TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway

Translational Oncology

Qian sun¹  Lun Gao¹  Hongxiang Jiang¹  Qianxue Chen¹  Linyao Zhao¹  Shiao Tong¹  Yong Li¹  Zhang Ye²  Jiayang Cai²  Si Zhang²  Ji'an Yang²  Yixuan Wang²  Yang Xu²  Tengfeng Yan² 

[1] Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei, China, 430060;Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, China, 430060;

关键词: TMBIM1;    p38 MAPK;    Proliferation;    Apoptosis;    Glioblastoma;   

DOI  :  

来源: DOAJ

【 摘 要 】

Glioblastoma multiforme (GBM) is the most common and most fatal primary malignant brain tumour in adults. The average survival time of patients after diagnosis is only 12–15 months. And its characteristics of excessive proliferation and apoptosis evasion play a crucial role in the poor prognosis of patients. Therefore, it is worth investigating the molecular mechanism of GBM to find an effective therapeutic target to overcome the dilemma. In the current study, Transmembrane BAX inhibitor motif containing 1 (TMBIM1) was highly expressed in GBM tissues and high TMBIM1 expression in GBM cell lines (U87 and U251) could promote cell proliferation and inhibit cell cycle arrest. In addition, TMBIM1 could significantly attenuate GBM cell apoptosis and decrease the sensitivity of GBM cells to temozolomide (TMZ). In terms of the molecular mechanism, we revealed that TMBIM1 interferes with the p38/MAPK pathway by inhibiting p38 phosphorylation to promote cell proliferation and attenuate cell apoptosis. In vivo experiments showed that the survival time of mice in TMBIM1 knockdown group was significantly prolonged. Our discovery provided an important basis for future intensive molecular mechanism research in GBM and presented a potential target for the treatment of GBM.

【 授权许可】

Unknown