[MiR-6838-5p overexpression inhibits proliferation of breast cancer MCF-7 cells by downregulating DDR1 expression].

Objective: To explore the regulatory effect of miR-6838-5p on DDR1 gene expression and proliferation of breast cancer cells.

Methods: The expression levels of miR-6838-5p in normal breast epithelial cells and breast cancer cells were detected using qRT-PCR, and the potential target genes of miR-6838-5p was predicted using TargetscanV 8.0. Double luciferase reporter gene experiment was performed to verify the binding between miR-6838-5p and DDR1. Breast cancer MCF-7 cells were transfected via liposome, miR-6838-5p mimic, miR-6838-5p inhibitor, DDR1 siRNA, DDR1-overexpresisng vector, or both miR-6838-5p mimic and DDR1-overexpressing vector, and the changes in cell proliferation were examined with CCK-8 and EdU assays; Western blotting was used to detect the expression of DDR1. The mediating role of DDR1 in miR-6838-5p overexpression-induced inhibition of MCF-7 cell proliferation was verified in a nude mouse model bearing MCF-7 cell xenografts.

Results: The expression of miR-6838-5p was significantly lower in breast cancer cells than in normal breast epithelial cells. In MCF-7 cells, miR-6838-5p overexpression induced significant inhibition of cell proliferation. Dual luciferase reporter gene experiment demonstrated a binding relationship between miR-6838-5p and DDR1 (P < 0.01). Western blotting showed that miR-6838-5p overexpression significantly lowered DDR1 expression in MCF-7 cells, and DDR1 overexpression promoted proliferation of the cells; co-transfection of the cells with DDR1-overexpressing vector significantly attenuated the inhibitory effect of miR-6838-5p mimic on cell proliferation. In the tumor-bearing nude mice, the xenografts overexpressing miR-6838-5p showed a significantly smaller volum with obviously the expression of DDR1.

Conclusion: Overexpression of miR-6838-5p inhibits breast cancer cell proliferation by regulating DDR1 expression.