MiR-93-5p inhibits the EMT of breast cancer cells via targeting MKL-1 and STAT3

Exp Cell Res. 2017 Aug 1;357(1):135-144. doi: 10.1016/j.yexcr.2017.05.007. Epub 2017 May 9.

Abstract

Epithelial-mesenchymal transition (EMT) plays an important role in breast cancer cell metastasis. Both (megakaryoblastic leukemia)/myocardin-like 1 (MKL-1) and Signal transducer and activator of transcription 3 (STAT3) have been implicated in the control of cellular metabolism, survival and growth. Our previous study has shown that cooperativity of MKL-1 and STAT3 promoted breast cancer cell migration. Herein, we demonstrate a requirement for MKL-1 and STAT3 in miRNA-mediated cellular EMT to affect breast cancer cell migration. Here we show that cooperativity of MKL-1 and STAT3 promoted the EMT of MCF-7 cells. Importantly, MKL-1 and STAT3 promoted the expression of Vimentin via its promoter CArG box. Interestingly, miR-93-5p inhibits the EMT of breast cancer cells through suppressing the expression of MKL-1 and STAT3 via targeted their 3'UTR. These results demonstrated a novel pathway through which miR-93-5p regulates MKL-1 and STAT3 to affect EMT controlling breast cancer cell migration.

Keywords: EMT; MKL-1; STAT3; The migration breast cancer cells; miR-93-5p.

MeSH terms

  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism
  • Epithelial-Mesenchymal Transition / physiology*
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • MCF-7 Cells
  • MicroRNAs / genetics*
  • Promoter Regions, Genetic / genetics
  • STAT3 Transcription Factor / genetics*
  • Trans-Activators / genetics*

Substances

  • MIRN93 microRNA, human
  • MRTFA protein, human
  • MicroRNAs
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Trans-Activators