Fig. 1

The multiple pathways for DNA damage repair, cell cycle arrest, and apoptosis escape after radiation therapy. Key regulators in the DNA damage repair pathway may alter sensitivity to radiotherapy in cancer cells, whereas cell cycle checkpoints may respond to damage when tumor cells are exposed to ionizing radiation, thus causing cell cycle arrest and allowing more time for repair, which increases resistance to radiotherapy. If DNA damage repair is unsuccessful, apoptotic signaling pathways are induced to resist radiotherapy damage. HR: homologous recombination, NHEJ: non-homologous end joining, BER: base excision repair DSBs: double-strand breaks, SSBs: single-strand breaks, ATM: ataxia-telangiectasia mutated, ATR: ATM and Rad3-related kinase, DNA-PKcs: DNA-dependent protein kinase, MRN: Mre11–Rad50–NBS1, RPA: replication protein A, DNA-PKcs: DNA-dependent protein kinase catalytic subunit, CHK1: checkpoint kinase 1, CHK2: checkpoint kinase 2, PARP: poly(ADP-ribose) polymerase, XRCC4: X-ray repair cross-complementing protein 4, XLF:XRCC4-like factor, PAXX: Paralogue of XRCC4 and XLF, LIG4: DNA ligase IV, MDC1: mediator of DNA damage checkpoint protein 1, CAD: caspase-activated DNase, ICAD: inhibitor of CAD, MDM2: mouse double minute 2 homolog, FBXW7: F-box and WD repeat domain-containing 7, BCL-2: B-cell lymphoma 2