MicroRNAs (miRNAs) are involved in multiple skin pathologies, including wound healing. Here, we explored the detailed role and molecular mechanism of miR-132 on HaCaT cells proliferation and migration. qRT-PCR assay was used to assess miR-132 expression and Western blot analysis was performed to detect inhibitor of matrix metalloproteinase-3 (TIMP3) level in HaCaT cells and normal human epidermal keratinocytes (NHEK) under transforming growth factor β1 (TGF-β1) treatment. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to confirm the endogenous interaction between miR-132 and TIMP3. Cell proliferation ability was determined by MTT assay and the migration capacity was evaluated by transwell assay. TGF-β1 treatment resulted in a increase of miR-132 expression and a decrease of TIMP3 level in HaCaT cells and NHEK cells. The proliferation and migration abilities of TGF-β1-treated HaCaT cells were promoted by miR-132 upregulation, while them were inhibited by TIMP3 overexpression. Moreover, TIMP3 was a direct target of miR-132. MiR-132-mediated pro-proliferation and pro-migration effects were antagonized by TIMP3 in HaCaT cells under TGF-β1 treatment. Our data supported that miR-132 promoted the proliferation and migration of HaCaT cells at least partly by targeting TIMP3, highlighting miR-132 as a potential therapeutic strategy of wound healing.
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