Bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway

Glioblastoma multiforme (GBM) is the most prevalent and lethal primary intracranial neoplasm in the adult population, with treatments of limited efficacy. Recently, bufotalin has been shown to have anti-cancer activity in a variety of cancers. This investigation aims to investigate the effect of buf...

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Bibliographic Details
Published in:Aging (Albany, NY.) NY.), 2024-05, Vol.16 (10), p.9264-9279
Main Authors: Zhu, Zhansheng, Liang, Shanwen, Hong, Yu, Qi, Yangzhi, Sun, Qian, Zhu, Xinyi, Wei, Yuxin, Xu, Yang, Chen, Qianxue
Format: Article
Language:English
Subjects:
Animals
Apoptosis - drug effects
Brain Neoplasms - drug therapy
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Bufanolides - pharmacology
Bufanolides - therapeutic use
Cell Line, Tumor
Cell Proliferation - drug effects
Epithelial-Mesenchymal Transition - drug effects
Glioblastoma - drug therapy
Glioblastoma - metabolism
Glioblastoma - pathology
Humans
Mice
Mitochondria - drug effects
Mitochondria - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Reactive Oxygen Species - metabolism
Research Paper
Signal Transduction - drug effects
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Summary:Glioblastoma multiforme (GBM) is the most prevalent and lethal primary intracranial neoplasm in the adult population, with treatments of limited efficacy. Recently, bufotalin has been shown to have anti-cancer activity in a variety of cancers. This investigation aims to investigate the effect of bufotalin on GBM and elucidate its potential underlying mechanism. Our results show that bufotalin not only inhibits the proliferation and epithelial-mesenchymal transition (EMT) but also triggers apoptosis in GBM cells. The result of RNA-seq indicated that bufotalin could induce mitochondrial dysfunction. Moreover, our observations indicate that bufotalin induces an excessive accumulation of intracellular reactive oxygen species (ROS) in GBM cells, leading to mitochondrial dysfunction and the dephosphorylation of AKT. Moreover, bufotalin improved TMZ sensitivity of GBM cells and . In conclusion, bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway.
ISSN:1945-4589
1945-4589
DOI:10.18632/aging.205883