MiR-106a inhibits glioma cell growth by targeting E2F1 independent of p53 status
journal contributionposted on 21.03.2012 by Guang Yang, Ruyou Zhang, Xiaofeng Chen, Yulong Mu, Jing Ai, Chen Shi, Yaohua Liu, Changbin Shi, Lihua Sun, Nikolai G. Rainov, Hulun Li, Baofeng Yang, Shiguang Zhao
Any type of content formally published in an academic journal, usually following a peer-review process.
MicroRNAs are single-stranded small non-coding RNA molecules which regulate mammalian cell growth, differentiation, and apoptosis by altering the expression of other genes and play a role in tumor genesis and progression. MiR-106a is upregulated in several types of malignancies and provides a pro-tumorigenic effect. However, its role in glioma is largely unknown. Our findings demonstrate that the low expression of miR-106a in human glioma specimens is significantly correlated with high levels of E2F1 protein and high-grade glioma. Here, we present the first evidence that miR-106a provides a tumor-suppressive effect via suppressing proliferation of and inducing apoptosis in human glioma cells. We further show that E2F1 is a direct functional target of miR-106a, suggesting that the effect of miR-106a on the glioma suppressive effect may result from inhibition of E2F1 via post-transcriptional regulation. In addition, our results reveal that miR-106a can increase p53 expression via E2F1 inhibition, whereas the effect of miR-106a on the proliferation of glioma cells is independent of p53 status. Further investigations will focus on the therapeutic use of miR-106a-mediated antitumor effects in glioma.