miR-135 regulated breast cancer proliferation and epithelial-mesenchymal transition acts by the Wnt/β-catenin signaling pathway.

Breast cancer (BC) is the most common cancer in women around the world. microRNAs (miRNAs/miRs) have been proved to be associated with the development and progression of breast cancer. In the present study, to elucidate the effects of dysregulated miR‑135 on cells and underlying mechanisms in BC, in vitro and in vivo experiments were conducted. The biological functions of miR‑135 were studied using MTT, colony formation, wound healing, transwell assays as well as tumorigenicity analysis. Gain‑ and loss‑ of function of miR‑135 studies revealed that ectopic expression of miR‑135 in MDA‑MB‑468 and MCF‑7 cells significantly inhibited cell growth, migration, invasion and EMT, at least in part through inhibiting the activation of the Wnt/β‑catenin pathway. Moreover, this was reversed in cells which were transfected with miR‑135 inhibitors. Taken together, the results of the present study provided evidence that miR‑135 acted as a tumor suppressor in BC, which may represent a novel therapeutic strategy for the diagnosis and prognosis of BC.