miR-21-mediated Radioresistance Occurs via Promoting Repair of DNA Double Strand Breaks.

摘要: miR-21, as an oncogene that overexpresses in most human tumors, is involved radioresistance; however, the mechanism remains unclear. Here, we demonstrate 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 (HRR). The miR-21-promoted NHEJ targeting GSK3B (a novel target miR-21), affects CRY2/PP5 pathway turn increases DNA-PKcs activity. HRR CDC25A known neutralizes effects GSK3B-induced increase because promotes degradation cyclin D1, but D1 have opposite effect on HRR. A negative correlation expression levels between miR-21 GSK3β exists a subset tumors. Our results not only elucidate radioresistance, also provide potential new targets for improving radiotherapy.