miR-200c enhances radiosensitivity of human breast cancer cells

被引:92
作者
Lin, Jing [1 ]
Liu, Cong [1 ]
Gao, Fu [1 ]
Mitchel, R. E. J. [2 ]
Zhao, Luqian [1 ]
Yang, Yanyong [1 ]
Lei, Jixiao [1 ]
Cai, Jianming [1 ]
机构
[1] Second Mil Med Univ, Dept Radiat Med, Fac Naval Med, Shanghai 200433, Peoples R China
[2] Atom Energy Canada Ltd, Radiol Protect Res & Instrumentat Branch, Chalk River Labs, Chalk River, ON K0J 1J0, Canada
基金
中国国家自然科学基金;
关键词
miR-200c; RADIATION THERAPY; RADIOSENSITIVITY; BREAST CANCER; TBK1; DOWN-REGULATION; MESENCHYMAL TRANSITION; HISTONE H2AX; DNA-DAMAGE; RADIATION; EXPRESSION; ZEB1; APOPTOSIS; FAMILY; TBK1;
D O I
10.1002/jcb.24398
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 epithelialmesenchymal 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. J. Cell. Biochem. 114: 606615, 2013. (C) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:606 / 615
页数:10
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