To investigate the role of miR-17-5p in mediating cisplatin（DDP）resistance in breast cancer cells by regulating the PTEN/Akt pathway.

MCF-7/DDP-resistant cell line was cultured with a gradient of increasing DDP concentrations. The content of miR-17-5p was detected in MCF-7 and MCF-7/DDP cells by RT-qPCR. MCF-7 cells were divided into miR-NC and miR-17-5p groups, and transfected with miR-NC and miR-17-5p mimics plasmids,respectively. MCF-7/DDP-resistant cells were divided into anti-miR-NC and anti-miR-17-5p groups, and transfected with anti-miR-NC and anti-miR-17-5p plasmids, respectively. Transfection efficiency was defined by RT-qPCR. The drug sensitivity of DDP in each group of transfected cells was evaluated by MTT. The direct effect of miR-17-5p on the invasive ability was obtained by Transwell assay. DDP-induced apoptosis of MCF-7 and MCF-7/DDP cells after transfection was analyzed by flow cytometry. The targeting relationship between miR-17-5p and PTEN was verified by double luciferase reporter gene assay. The changes of apoptosis and key proteins of PTEN/Akt pathway under the regulation of miR-17-5p were detected by Western blot.

Compared with MCF-7 cells, the miR-17-5p expression in MCF-7/DDP-resistant cells was abnormally increased, while the PTEN expression was reduced（P<0.01）. PTEN was regulated by miR-17-5p as a target gene. Compared with the miR-NC group, the proliferation inhibition rate in the miR-17-5p mimics group was significantly declined, the number of invaded cells was enhanced, and the apoptosis rate was also decreased（P<0.05）, and the expressions of tumor suppressor proteins PTEN, p21 and p27 in the PTEN/Akt pathway were decreased, and the expressions of p-Akt308, p-Akt473 and cyclin D1 were increased（P<0.01）. Compared with the anti-miR-NC group, the proliferation inhibition rate was increased in the anti-miR-17-5p group, the number of invaded cells was decreased, and the apoptosis rate was also increased（P<0.05）, and the expression of tumor suppressor proteins PTEN, p21 and p27 was increased, and the expression of p-Akt308, p-Akt473 and cyclin D1 was decreased（P<0.01）.

Knockdown of miR-17-5p can effectively improve the DDP sensitivity of breast cancer cells, attenuate the invasive ability, and induce further apoptosis,which may be related to the regulatory effect of miR-17-5p on the PTEN/Akt pathway.