MicroRNA-129-3p suppresses tumor growth by targeting E2F5 in glioblastoma.

OBJECTIVE: Neuroma is the most common intracranial tumor. The mechanism of miRNA in glioma has gradually been understood. The purpose of this study was to investigate the role of MicroRNA-129-3p (miR-129-3p) in the pathogenesis of glioblastoma (GBM). PATIENTS AND METHODS: Differential expression of miR-129-3p in samples was analyzed by bioinformatics. PCR was used to detect the expression of miR-129-3p in samples. CCK8 assay was used to detect the cell viability. Transfection of mimic and inhibitor altered the expression of miR-129-3p, and the biological function of miRNA was explored. Luciferase reporter gene was used to detect target genes of miRNA. E2F5 expression was inhibited by transfection of small interfering RNAs. Western blotting was used to detect protein expressions of cells. RESULTS: miR-129-3p was low-expressed in the tissue samples. By transfecting mimic and the inhibitor, we found that increasing the expression of miR-129-3p can inhibit the cell viability. In contrast, inhibition of miR-129-3p promoted cell growth. Luciferase reporter gene and Western blot results suggested that E2F5 can be used as the target gene of miR-129-3p. Knockdown the target gene of the miR-129-3p, E2F5, also inhibited proliferation of glioblastoma. CONCLUSIONS: miR-129-3p can inhibit the growth of glioblastoma by down-regulating the expression of E2F5. miR-129-3p can be a new target for the treatment of glioblastoma. Our research provides new ideas for the target therapy of glioma.

miR-98 delays skeletal muscle differentiation by down-regulating E2F5.

A genome-wide screen had previously shown that knocking down miR-98 and let-7g, two miRNAs of the let-7 family, leads to a dramatic increase in terminal myogenic differentiation. In the present paper, we report that a transcriptomic analysis of human myoblasts, where miR-98 was knocked down, revealed that approximately 240 genes were sensitive to miR-98 depletion. Among these potential targets of miR-98, we identified the transcriptional repressor E2F5 and showed that it is a direct target of miR-98. Knocking down simultaneously E2F5 and miR-98 almost fully restored normal differentiation, indicating that E2F5 is involved in the regulation of skeletal muscle differentiation. We subsequently show that E2F5 can bind to the promoters of two inhibitors of terminal muscle differentiation, ID1 (inhibitor of DNA binding 1) and HMOX1 (heme oxygenase 1), which decreases their expression in skeletal myoblasts. We conclude that miR-98 regulates muscle differentiation by altering the expression of the transcription factor E2F5 and, in turn, of multiple E2F5 targets.