Background: Breast cancer affects millions of people with a high mortality rate throughout the world; microRNA 543 (miR-543) has been reported to suppress progression in some kinds of cancers, but has not been reported in breast cancer. Thus, the purpose of this study is to investigate the function of miR-543 in breast cancer cells.
Methods: Two cell lines, MCF-7 and MDA-MB-231, were selected to be the research objects; the miR-543 overexpression and knockdown models were established in the study by transforming miR-543 mimics and miR-543 inhibitor. Real-time polymerase chain reaction, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Western blot, clone formation and cell flow cytometer assay were used to test the miR-543’s function. Dual-luciferase assay was used for the detection of miR-543 and ERK2 targeting relationship.
Results: The results showed that the cell proliferation and cell cycle were inhibited, and the capability of cell apoptosis was upregulated when miR-543 was overexpressed; we found that there was a target relationship between ERK2 and miR-543. Furthermore, downstream factors of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-2 (ERK2) pathway, including RSK2 and MSK1, were decreased in miR-543 overexpression model.
Conclusion: This study provides series evidences to support that breast cancer progression was inhibited by miR-543 via direct targeting of ERK2 in MAPK/ERK signal pathway, which may provide a molecular basis for better treatment for patients.
Keywords: microRNA 543, breast cancer, ERK2, apoptosis, cell cycle, proliferation