Due to the intrinsic resistance of many tumors to radiotherapy, current methods to improve the survival of cancer patients largely depend on increasing tumor radiosensitivity. It is well-known that miR-200c inhibits epithelial-mesenchymal transition (EMT), and enhances cancer cell chemosensitivity. We sought to clarify the effects of miR-200c on the radiosensitization of human breast cancer cells. In this study, we found that low levels of miR-200c expression correlated with radiotolerance in breast cancer cells. miR-200c overexpression could increase radiosensitivity in breast cancer cells by inhibiting cell proliferation, and by increasing apoptosis and DNA double-strand breaks. Additionally, we found that miR-200c directly targeted TANK-binding kinase 1 (TBK1). However, overexpression of TBK1 partially rescued miR-200c mediated apoptosis induced by ionizing radiation. In summary, miR-200c can be a potential target for enhancing the effect of radiation treatment on breast cancer cells.
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