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

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...

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Autores principales: Cai, Jiayang, Gao, Lun, Wang, Yixuan, Li, Yong, Ye, Zhang, Tong, Shiao, Yan, Tengfeng, sun, Qian, Xu, Yang, Jiang, Hongxiang, Zhang, Si, Zhao, Linyao, Yang, Ji'an, Chen, Qianxue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Neoplasia Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8920937/
https://www.ncbi.nlm.nih.gov/pubmed/35279540
http://dx.doi.org/10.1016/j.tranon.2022.101391
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author Cai, Jiayang
Gao, Lun
Wang, Yixuan
Li, Yong
Ye, Zhang
Tong, Shiao
Yan, Tengfeng
sun, Qian
Xu, Yang
Jiang, Hongxiang
Zhang, Si
Zhao, Linyao
Yang, Ji'an
Chen, Qianxue
author_facet Cai, Jiayang
Gao, Lun
Wang, Yixuan
Li, Yong
Ye, Zhang
Tong, Shiao
Yan, Tengfeng
sun, Qian
Xu, Yang
Jiang, Hongxiang
Zhang, Si
Zhao, Linyao
Yang, Ji'an
Chen, Qianxue
author_sort Cai, Jiayang
collection PubMed
description 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.
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spelling pubmed-89209372022-03-21 TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway Cai, Jiayang Gao, Lun Wang, Yixuan Li, Yong Ye, Zhang Tong, Shiao Yan, Tengfeng sun, Qian Xu, Yang Jiang, Hongxiang Zhang, Si Zhao, Linyao Yang, Ji'an Chen, Qianxue Transl Oncol Original Research 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. Neoplasia Press 2022-03-10 /pmc/articles/PMC8920937/ /pubmed/35279540 http://dx.doi.org/10.1016/j.tranon.2022.101391 Text en © 2022 The Authors. Published by Elsevier Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Research
Cai, Jiayang
Gao, Lun
Wang, Yixuan
Li, Yong
Ye, Zhang
Tong, Shiao
Yan, Tengfeng
sun, Qian
Xu, Yang
Jiang, Hongxiang
Zhang, Si
Zhao, Linyao
Yang, Ji'an
Chen, Qianxue
TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title_full TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title_fullStr TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title_full_unstemmed TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title_short TMBIM1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 MAPK signalling pathway
title_sort tmbim1 promotes proliferation and attenuates apoptosis in glioblastoma cells by targeting the p38 mapk signalling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8920937/
https://www.ncbi.nlm.nih.gov/pubmed/35279540
http://dx.doi.org/10.1016/j.tranon.2022.101391
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