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• W2947320259 abstract "Hypoxia is a key driver of tumor adaptation being involved in tumor progression as well in resistance to therapy. Hypoxia-dependent factors could be attractive therapeutic targets in GBM management, that up to date is characterized by a poor prognosis. Several molecular mechanisms have been investigated to explain the anti-cancer effects of MET in GBM. Here, we found that MET, in combination with TMZ standard therapy, could improve the chemo-sensitivity and overall could revert the chemoresistance also in hypoxic condition. COMBO was indeed able to induce a sensitive-like pattern of the apoptotic genes in TMZ-resistant cells, reducing cell viability. Moreover, we assessed HIF-1 modulation and the potential role exerted by PI3k/AKT pathway. In U251, COMBO produced a marked decrease of stem cell markers, HIF-1α levels and AKT activation inducing a pro-apoptotic phenotype. In T98 cells, COMBO failed to reduce the hypoxia-dependent increase in CD133 positive cells. The administration of the dual PI3K/mTOR inhibitor BEZ235 potentiated the effect of COMBO on cell viability during hypoxic conditions suggesting the block of the PI3k/AKT pathway as a complementary target to further overcome GBM resistance." @default.
• W2947320259 created "2019-06-07" @default.
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• W2947320259 date "2019-05-31" @default.
• W2947320259 modified "2023-10-18" @default.
• W2947320259 title "Role of Metformin and AKT Axis Modulation in the Reversion of Hypoxia Induced TMZ-Resistance in Glioma Cells" @default.
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• W2947320259 doi "https://doi.org/10.3389/fonc.2019.00463" @default.
• W2947320259 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6554426" @default.
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