Retracted Article: MiR-132 enhances proliferation and migration of HaCaT cells by targeting TIMP3.

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.