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Bax Activation Blocks Self-Renewal and Induces Apoptosis of Human Glioblastoma Stem Cells

Bax Activation Blocks Self-Renewal and Induces Apoptosis of Human Glioblastoma Stem Cells

Simona Daniele, Deborah Pietrobono, Barbara Costa, Mariateresa Giustiniano, Valeria La Pietra, Chiara Giacomelli, Giuseppe La Regina, Romano Silvestri, Sabrina Taliani, Maria Letizia Trincavelli, Federico Da Settimo, etc.

ACS Chem Neurosci. 2018 Jan 17;9(1):85-99.

PMID: 28368610

Abstract:

Glioblastoma (GBM) is characterized by a poor response to conventional chemotherapeutic agents, attributed to the insurgence of drug resistance mechanisms and to the presence of a subpopulation of glioma stem cells (GSCs). GBM cells and GSCs present, among others, an overexpression of antiapoptotic proteins and an inhibition of pro-apoptotic ones, which help to escape apoptosis. Among pro-apoptotic inducers, the Bcl-2 family protein Bax has recently emerged as a promising new target in cancer therapy along with first BAX activators (BAM7, Compound 106, and SMBA1). Herein, a derivative of BAM-7, named BTC-8, was employed to explore the effects of Bax activation in different human GBM cells and in their stem cell subpopulation. BTC-8 inhibited GBM cell proliferation, arrested the cell cycle, and induced apoptosis through the induction of mitochondrial membrane permeabilization. Most importantly, BTC-8 blocked proliferation and self-renewal of GSCs and induced their apoptosis. Notably, BTC-8 was demonstrated to sensitize both GBM cells and GSCs to the alkylating agent Temozolomide. Overall, our findings shed light on the effects and the relative molecular mechanisms related to Bax activation in GBM, and they suggest Bax-targeting compounds as promising therapeutic tools against the GSC reservoir.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP331244894	BAM7		331244-89-4	Price
AP906440377	SMBA1		906440-37-7	Price

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