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Bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway.
- Source :
-
Aging [Aging (Albany NY)] 2024 May 28; Vol. 16 (10), pp. 9264-9279. Date of Electronic Publication: 2024 May 28. - Publication Year :
- 2024
-
Abstract
- 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 in vitro and in vivo . In conclusion, bufotalin enhances apoptosis and TMZ chemosensitivity of glioblastoma cells by promoting mitochondrial dysfunction via AKT signaling pathway.
- Subjects :
- Humans
Cell Line, Tumor
Animals
Cell Proliferation drug effects
Mice
Brain Neoplasms drug therapy
Brain Neoplasms metabolism
Brain Neoplasms pathology
Epithelial-Mesenchymal Transition drug effects
Glioblastoma drug therapy
Glioblastoma metabolism
Glioblastoma pathology
Apoptosis drug effects
Mitochondria drug effects
Mitochondria metabolism
Proto-Oncogene Proteins c-akt metabolism
Signal Transduction drug effects
Bufanolides pharmacology
Bufanolides therapeutic use
Reactive Oxygen Species metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1945-4589
- Volume :
- 16
- Issue :
- 10
- Database :
- MEDLINE
- Journal :
- Aging
- Publication Type :
- Academic Journal
- Accession number :
- 38809514
- Full Text :
- https://doi.org/10.18632/aging.205883