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Skin scar is a common cutaneous complication, the outcome of which is unpleasant. Several microRNAs (miRs) participate in the process of skin scar formation. We aimed to explore the role of miR-27a-3p in NIH/3T3 mouse fibroblasts as well as the downstream protein and signaling cascades.    Material and methods  miR-27a-3p was aberrantly expressed in NIH/3T3 cells, followed by measurements of cell viability, migration and expressions of proteins related to proliferation and migration. Perlecan expression in cells aberrantly expressing miR-27a-3p was examined by Western blot analysis. Reporter gene assay was conducted to assess the relationship between miR-27a-3p and perlecan. Then, whether miR-27a-3p affected NIH/3T3 cells through regulating perlecan was ascertained. The effects of aberrantly expressed miR-27a-3p and perlecan on expression levels of VEGF, bFGF and key kinases in the MAPK/ERK and the PI3K/AKT pathways were detected.    Results  Cell viability and migration were enhanced and protein expression levels of Cyclin D1, MMP-2 and MMP-9 were up-regulated by miR-27a-3p overexpression in NIH/3T3 cells. Then, we found that perlecan was positively correlated with miR-27a-3p expression, and its knockdown abrogated the effects of miR-27a-3p overexpression on NIH/3T3 cells. Finally, we found that the expression levels of VEGF and bFGF as well as phosphorylated levels of MAPK, ERK, PI3K and AKT were increased by miR-27a-3p overexpression, and those increases were reversed by perlecan knockdown.    Conclusions  miR-27a-3p promotes proliferation and migration of NIH/3T3 cells through up-regulating perlecan expression. Meanwhile, miR-27a-3p up-regulates expression levels of VEGF and bFGF, and activates MAPK/ERK and PI3K/AKT pathways through up-regulating perlecan expression.

MicroRNA-27a-3p promotes proliferation and migration by up-regulation of perlecan in murine fibroblast cell line NIH/3T3