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A previous study showed that miR-221/222 can regulate cell apoptosis. p53is a well known tumor suppressor which can influence the chemosensitivity of gliomacells. However, the effect of miR-221/222 in gliomas with different p53 statusis unknown. Here, we demostrate that knockdown of miR-221/222 increases apoptosisin human gliomas of different p53 types (U251 cells, p53 mutant-type; LN308 cells,p53 null-type; and U87 cells, p53 wild-type). Furthermore, the effect of miR-221/22caused no change of p53 expression in the glioma cells studied. In addition, whena specific siRNA against p53 was employed in U87 cells, no attenuation of apoptosiswas found after knockdown of miR-221/222. Importantly, we found that As-miR-221/222-treatedcells increased expression of Bax, cytochrome c, Apaf-1 and cleaved-caspase-3.Our results showed that low expression of miR-221/222 sensitized glioma cellsto temozolomide (TMZ); in addition, ectopic expression of PUMA by pcDNA-PUMA hada similar effect. Taken together, our study indicates that downregulated miR-221/222can sensitize glioma cells to TMZ by regulating apoptosis independently of p53status.

Downregulation of miR-221/222 sensitizes glioma cells to temozolomide by regulating apoptosis independently of p53 status