MIR-17-5P INHIBITS THE PROLIFERATION AND MIGRATION OF BREAST CANCER CELLS BY TARGETING ARHGAP1

Objective: The purpose of this study was to investigate the regulatory mechanism of miR-17-5p in inhibiting the proliferation and migration of breast cancer cells by targeting ARHGAP1. Methods: We analyzed the expression of ARHGAP1 and miR-17-5p in breast cancer tissues and normal tissues through the GEO database GEO2R analysis and the UALCAN database. The binding site of miR-17-5p to ARHGAP1 was predicted using the bioinformatics websites Starbase and TargetScan. The expression of miR-17-5p in breast cancer cell lines was evaluated by quantitative real-time PCR (qRT-PCR). The expression of ARHGAP1 in breast cancer cells was detected by qRT-PCR and Western blotting. The proliferation capacity of breast cancer cells in each group was determined using cell count Kit 8 (CCK-8). The colony formation ability of breast cancer cells in each group was detected by colony formation. The cell scratch test was used to detect the migration ability of breast cancer cells in each group. The targeting relationship between miR-17-5p and ARHGAP1 was verified by the double luciferase reporter gene experiment. Results: The results of data analysis showed that the expression of miR-17-5p was significantly decreased in breast cancer cell lines and clinical breast cancer tissues. Meanwhile, the overexpression of miR-17-5p in vitro significantly inhibited the proliferation, colony formation and invasion of breast cancer cells. In contrast, the expression of ARHGAP1 was significantly up-regulated in breast cancer cell lines and tissues, and the expression of miR-17-5p was significantly inversely correlated with ARHGAP1. The luciferase reporter gene assay confirmed that ARHGAP1 was a direct target of miR-17-5p. At the same time, forced overexpression of ARHGAP1 in HCC197 and MCF-7 cells significantly promoted cell proliferation, colony formation and in vitro migration. Conclusion: In summary, our study suggests that miR-17-5p expression is associated with a good prognosis in breast cancer and significantly affects cell proliferation and migration. ARHGAP1 was the target gene of miR-17-5p and was involved in the regulation of miR-17-5p on cell proliferation and migration. Our data provide new insights into the diagnosis and molecular therapy of breast cancer.