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miR-21-mediated Radioresistance Occurs via Promoting Repair of DNA Double Strand Breaks.
Hu, Baocheng; Wang, Xiang; Hu, Shuofeng; Ying, Xiaomin; Wang, Ping; Zhang, Xiangming; Wang, Jian; Wang, Hongyan; Wang, Ya.
Afiliación
  • Hu B; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Wang X; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Hu S; Beijing Institute of Basic Medical Sciences, Beijing 100850, China.
  • Ying X; Beijing Institute of Basic Medical Sciences, Beijing 100850, China.
  • Wang P; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Zhang X; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Wang J; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Wang H; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322.
  • Wang Y; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, Georgia 30322. Electronic address: ywang94@emory.edu.
J Biol Chem ; 292(8): 3531-3540, 2017 02 24.
Article en En | MEDLINE | ID: mdl-28096467
miR-21, as an oncogene that overexpresses in most human tumors, is involved in radioresistance; however, the mechanism remains unclear. Here, we demonstrate that miR-21-mediated radioresistance occurs through promoting repair of DNA double strand breaks, which includes facilitating both non-homologous end-joining (NHEJ) and homologous recombination repair (HRR). The miR-21-promoted NHEJ occurs through targeting GSK3B (a novel target of miR-21), which affects the CRY2/PP5 pathway and in turn increases DNA-PKcs activity. The miR-21-promoted HRR occurs through targeting both GSK3B and CDC25A (a known target of miR-21), which neutralizes the effects of targeting GSK3B-induced CDC25A increase because GSK3B promotes degradation of both CDC25A and cyclin D1, but CDC25A and cyclin D1 have an opposite effect on HRR. A negative correlation of expression levels between miR-21 and GSK3ß exists in a subset of human tumors. Our results not only elucidate miR-21-mediated radioresistance, but also provide potential new targets for improving radiotherapy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación de la Expresión Génica / MicroARNs / Reparación del ADN / Roturas del ADN de Doble Cadena Límite: Animals / Humans Idioma: En Revista: J Biol Chem Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación de la Expresión Génica / MicroARNs / Reparación del ADN / Roturas del ADN de Doble Cadena Límite: Animals / Humans Idioma: En Revista: J Biol Chem Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos