Journal
EXPERIMENTAL CELL RESEARCH
Volume 357, Issue 1, Pages 135-144Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2017.05.007
Keywords
miR-93-5p; MKL-1; STAT3; EMT; The migration breast cancer cells
Categories
Funding
- National Natural Science Foundation of China [31501149, 31570764, 31401117, 31471282, 31440038, 31270837]
- Hubei Province Health and Family Planning Scientific Research Project [WJ2017M173]
- Science and Technology Young Training Program of the Wuhan University of Science and Technology [2016xz035, 2017xz027]
- innovation and entrepreneurship fund for Graduate of Wuhan University of Science and Technology
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available