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

Publication date: Available online 9 May 2017
Source:Experimental Cell Research
Author(s): Yuan Xiang, Xing-Hua Liao, Cheng-Xi Yu, Ao Yao, Huan Qin, Jia-Peng Li, Peng Hu, Hui Li, Wei Guo, Chao-Jiang Gu, Tong-Cun Zhang
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.



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