Effect of MicroRNA-766 Promotes Proliferation, Chemoresistance, Migration, and Invasion of Breast Cancer Cells

We studied the role of microRNA (miR)-766 in the proliferation and chemoresistance of breast cancer (BCa) using BCa cell lines. miR-766 regulated the proliferation, invasion, and migration of BCa cells by binding to 3' untranslated region of phosphatase and tensin homolog and regulating the phosphatase and tensin homolog signaling pathway. miR-766 could act as a potential biomarker to predict the chemosensitivity and prognosis in BCa. Introduction: Breast cancer (BCa) remains the most common cancer in women worldwide. It has been shown that microRNAs (miRs) play essential roles in tumorigenesis and progression in many types of cancers, including BCa. We assessed the role of miR-766 on the proliferation, chemosensitivity, migration, and invasion of BCa cells. Materials and Methods: The effect of miR-766 on the proliferation of MCF-7 and T47D BCa cells was evaluated using the MTT assay. The function of miR-766 on the migration and invasion of MCF-7 and T47D cells was examined using Transwell migration and Matrigel invasion assays. Protein expression was evaluated by Western blot. The role of miR-766 on 5-fluorouracil-induced apoptosis in MCF-7 and T47D cells was determined using the Caspase-Glo3/7 assay. A subcutaneous tumor xenograft was performed to examine the effect of miR-766 on tumor growth in vivo. Results: Upregulation of miR-766 improved the proliferation, invasion, and migration of BCa cells. Furthermore, miR-766 reduced the sensitivity of MCF-7 and T47D cells to 5-fluorouracil treatment. The tumor xenograft experiment showed that miR-766 promoted BCa growth in vivo. miR-766 decreased 5-flurouracil-induced apoptosis by regulation of BAX and Bcl-2 expression. miR-766 also affected the epitheliale-mesenchymal transition by altering E-cadherin, N-cadherin, SNAIL, and vimentin expression in MCF-7 and T47D cells. Further study showed that the expression of phosphatase and tensin homolog and phosphorylated AKT in MCF-7 and T47D cells had changed after aberrant expression of miR-766. Conclusion: miR-766 displayed important roles in tumorigenesis and progression in BCa cells and might act as a potential biomarker to predict the chemotherapy response and progression in BCa.