MiR-155 promotes the proliferation and migration of breast cancer cells via targeting SOCS1 and MMP16.

Abstract

The aim of this study was to investigate the effect of miR-155 on the proliferation and migration of breast cancer cells, and to explore the underlying mechanism. The breast cancer cell line MDA-MB-231 was transfected with miR-155 mimics, inhibitor or negative control, respectively. The expression level of miR-155 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Subsequently, the proliferation of MDA-MB-231 cells was detected by multi-cellular tumor spheroid (MTS) and colony formation assay. Cell migration was examined by transwell assay and scratch test. In addition, qRT-PCR was performed to analyze the expression of matrix metallopeptidase 16 (MMP16) after miR-155 mimics or inhibitor transfection in MDA-MB-231 cells. Meanwhile, Western blot was used to evaluate the protein expression levels of suppressor of cytokine signaling 1 (SOCS1) and MMP16 after miR-155 mimics or inhibitor transfection. QRT-PCR results showed that miR-155 mimics significantly increased the expression of miR-155 in MDA-MB-231 cells, whereas miR-155 inhibitor markedly decreased miR-155 expression (p < 0.05). Meanwhile, MTS and colony formation assay indicated that the proliferation of MDA-MB-231 cells was remarkably increased after miR-155 mimics transfection. However, miR-155 inhibitor transfection exhibited the opposite result in cell proliferation (p < 0.05). Moreover, miR-155 overexpression significantly increased the migration of MDA-MB-231 cells (p < 0.05). Western blot further confirmed that miR-155 overexpression down-regulated the expression level of target protein SOCS1 and upregulated the expression level of MMP16. We found that miR-155 significantly enhanced the proliferation and migration of MDA-MB-231 cells, which might serve as an oncogene in breast cancer. Therefore, it is preliminarily believed that miR-155 plays an important role in the proliferation and migration of breast cancer cells via down-regulating the expression of SOCS1 and up-regulating the expression of MMP16.