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.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Xiang Y,Liao XH,Yu CX,Yao A,Qin H,Li JP,Hu P,Li H,Guo W,Gu CJ,Zhang TCdoi
10.1016/j.yexcr.2017.05.007subject
Has Abstractpub_date
2017-08-01 00:00:00pages
135-144issue
1eissn
0014-4827issn
1090-2422pii
S0014-4827(17)30272-0journal_volume
357pub_type
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journal_title:Experimental cell research
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