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

- Cooperativity of MKL-1 and STAT3 promoted the EMT of MCF-7 cells.
- Cooperativity of MKL-1 and STAT3 promoted the expression of Vimentin via its promoter CArG box.
- MiR-93-5p inhibits the EMT of MCF-7 cells through suppressing MKL-1 and STAT3 via targeted their 3'UTR.

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.