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MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate proteinexpression by cleaving or repressing the translation of target mRNAs. miR-125b,one of the neuronal miRNAs, was recently found to be necessary for stem cell fissionand for making stem cells insensitive to chemotherapy signals. Temozolomide (TMZ)is a promising chemotherapeutic agent for treating glioblastomas. However, resistancedevelops quickly and with a high frequency. Given the insensitivity of some glioblastomasto TMZ and the hypothesis that glioma stem cells cause resistance to drug therapy,exploring the functions and mechanisms of miR-125b action on TMZ-treated glioblastomastem cells would be valuable. In this study, we found that miR-125b-2 is overexpressedin glioblastoma multiforme tissues and the corresponding stem cells (GBMSC); downregulationof miR-125b-2 expression in GBMSC could allow TMZ to induce GBMSC apoptosis. Additionally,the expression of the anti-apoptotic protein Bcl-2 was decreased after the TMZ+miR-125b-2inhibitor treatment, while the expression of the proapoptotic protein Bax wasincreased. Further research demonstrated that the induction of apoptosis in GBMSCis also associated with increased cytochrome c release from mitochondria, inductionof Apaf-1, activation of caspase-3 and poly-ADP-ribose polymerase (PARP). Takentogether, these results suggest that miR-125b-2 overexpression might confer glioblastomastem cells resistance to TMZ.

MicroRNA-125b-2 confers human glioblastoma stem cells resistance to temozolomide through the mitochondrial pathway of apoptosis