MiR-16 and miR-519 suppress tumor cell proliferation in meningiomas via HuR inhibition. Homo sapiens

We investigated the relative expression levels of these miRs in a series of meningioma and normal meningeal tissues. The effects of miR-16 and miR-519 on cell growth and transcriptome were assessed in vitro using two human cell lines (Ben-Men-1 and IOMM-Lee). Both miR-16 and miR-519 were significantly downregulated in meningioma compared with normal meningeal tissue. Overexpression of either miR in IOMM-Lee and Ben-Men-1 cells significantly reduced cell growth. The transfection of miR-16 and miR-519 significantly downregulated HuR mRNA, and genes involved in various functions such as pre-replicative complex, mitotic recombination, S phase and M phase of cell cycle, and upregulated genes implicated in cell junction, and positive regulation of cell death. Cell-cycle-related genes associated cluster included HuR mRNA (ELAVL1), and was highly enriched with HuR gene targets. Overall design: IOMM-Lee cells transfected with either miR Mimic hsa-miR-16-5p (miR16 ; n=6 ; biological replicates), miR Mimic hsa-miR-519a-3p (miR519 ; n=6 ; biological replicates) and mirVana miR Mimic Negative Control (ctrl ; n=6 ; biological replicates).