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Beclin 1 interacts with UV-irradiation-resistance-associated gene (UVRAG) to form core complexes that induce autophagy. While cells with defective autophagy are prone to genomic instability that contributes to tumorigenesis, it is unknown whether Beclin1 or UVRAG can regulate the DNA damage/repair response to cancer treatment in established tumor cells. We found that siRNA knockdown of  Beclin 1  or  UVRAG  can increase radiation-induced DNA double strand breaks (DSBs), shown by pATM and γH2Ax, and promote colorectal cancer cell death. Furthermore, knockdown of  Beclin 1 ,  UVRAG  or  ATG5  increased the percentage of irradiated cells with nuclear foci expressing 53BP1, a marker of nonhomologous end joining but not RAD51 (homologous recombination), compared to control siRNA.  Beclin 1  siRNA was shown to attenuate UVRAG expression. Cells with a  UVRAG  deletion mutant defective in Beclin 1 binding showed increased radiation-induced DSBs and cell death compared to cells with ectopic wild-type  UVRAG . Knockdown of  Beclin 1  or  UVRAG,  but not  ATG5,  resulted in a significant increase in centrosome number (γ-tubulin staining) in irradiated cells compared to control siRNA. Taken together, these data indicate that Beclin 1 and UVRAG confer protection against radiation-induced DNA DSBs and may maintain centrosome stability in established tumor cells.

Beclin 1 and UVRAG Confer Protection from Radiation-Induced DNA Damage and Maintain Centrosome Stability in Colorectal Cancer Cells