Abstract

Breast cancer remains the most commonly diagnosed cancer in Chinese women. Paclitaxel (PTX) is a chemotherapy medication used to treat breast cancer patients. However, a side effect of paclitaxel is the severe drug resistance. Previous studies demonstrated that dysregulation of microRNAs could regulate sensitivity to paclitaxel in breast cancer. Here, the present study aimed to lucubrate the underlying mechanisms of miR-107 in regulating the sensitivity of breast cancer cells to PTX. The results demonstrated that miR-107 was down-regulated in breast cancer tumor tissues, while TPD52 was significantly up-regulated compared with the non-tumor adjacent tissues. After confirming that TPD52 may be a major target of miR-107 via a dual-luciferase reporter assay, the western blot and RT-qPCR assays further demonstrated that miR-107 may reduce the expression level of TPD52 as well. In addition, miR-107 may prominently enhance PTX induced reduction of cell viability and the promotion of cell apoptosis in breast cancer, and the variation could be reversed by co-transfected with pcDNA3.1-TPD52. Finally, miR-107 could further reduce the decreased expression of TPD52, Wnt1, β-catenin and cyclin D1 that was induced by PTX in both mRNA and protein levels, which were rescued by pcDNA3.1-TPD52 indicating that miR-107 regulated breast cancer cell sensitivity to PTX may be targeting TPD52 through Wnt/β-catenin signaling pathway.