MiR-142-3p target hmgb1 reverses adriamycin resistance of breast cancer cell mcf-7 / 中国药理学通报

ABSTRACT

Aim To explore the molecular mechanism of miR-142-3p involved in the regulation of chemosen-sitivity of breast cancer by targeting high-mobility group box 1 ( HMGB1 ). Methods Real-time quantitative PCR ( QPCR) was employed to detect the levels of miR-142-3p in human breast cancer MCF-7 cells and doxorubicin-resistant MCF-7/D0X cells. MIT was used to detect the proliferation of doxorubicin ( DOX)-treated groups. Flow cytometry was applied to detect the apoptotic rate of each group after transfection. Western blot was used to detect the expression of HMGB1 and autophagy-related proteins. Double Lucif-erase Report experiment was carried out to evaluate the targeting effect of miR-142-3p on HMGB1. Results The level of miR-142-3p in MCF-7/D0X cells was sig nificantly down-regulated. Overexpression of miR-142-3p enhanced the sensitivity of breast cancer cells to DOX and increased the apoptotic rate induced by DOX. HMGB1 was the direct functional target of miR-142-3p in breast cancer cells,and the overexpression of HMGB1 could significantly relieve the promotion of ap-optosis and inhibition of autophagy by miR-142-3p uP-regulation. Conclusions The overexpression of miR-142-3p may enhance the chemosensitivity of breast cancer cells to DOX by inhibiting autophagy and targeting HMGB1. miR-142-3p/HMGBl provides a new target for reversing the drug resistance of breast cancer.