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Recent studies have revealed that miR-92a is overexpressed in several types of malignancies and provides a protumorigenic effect. Our findings demonstrate that the high expression of miR-92a in human glioma specimens is significantly correlated with low levels of BCL2L11 (Bim) protein and high-grade glioma. Here, we present the first evidence that miR-92a antisense oligonucleotide (AS-miR-92a) provides a tumor suppressive effect via induction of apoptosis in human glioma cells. In addition, we show that Bim is a direct functional target of miR-92a. Introducing Bim cDNA without 3'UTR abrogates miR-92a-induced cell survival. Further investigations will focus on the therapeutic use of AS-miR‑92a-mediated antitumor effects in glioma.

miR-92a is a critical regulator of the apoptosis pathway in glioblastoma with inverse expression of BCL2L11