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. Author manuscript; available in PMC: 2017 Nov 23.
Published in final edited form as: Trends Cancer. 2016 Nov 23;2(11):646–656. doi: 10.1016/j.trecan.2016.10.014

Figure 1. Hypoxia-Regulated DNA Repair.

Figure 1

During DNA replication, translation and transcription, as well as during epigenetic and post-translational modification, DNA is repaired using a number of pathways including HR, MMR, NER, BER, NHEJ, and TLS. DNA repair protein expression is sensitive to and modulated by hypoxia and oxia. In hypoxic conditions, DNA repair pathway protein expression is decreased in many instances, and NER, BER and NHEJ proteins involved in the DNA damage response are increased. The primary point of action for specific agents and inhibitors are indicated by repair pathways, damage response, and as a function of the stage of DNA replication and modification. During replication and repair, the hypoxic microenvironment may predispose to a loss of function phenotype.

Abbreviations: HR, homologous recombination; MMR, mismatch repair; NER, nucleotide excision repair; BER, base excision repair; NHEJ, non-homologous end joining; TLS, translesion synthesis; RAD51, RAD51 recombinase; BRCA2, BRCA2, DNA repair associated; RAD51B/C, RAD51 paralogs B and C; XRCC3, X-ray repair cross complementing 3; RAD52, RAD52 homolog DNA repair protein; MLH1, mutL homolog 1; PMS1, postmeiotic segregation increased 1; MSH6, mutS homolog 6; RAD23B, RAD23 homolog B; APE1, apurinic/apyrimidinic endonuclease 1; OGG1, 8-oxoguanine DNA glycosylase; MYH, mutY DNA glycosylase; NEIL2, nei like DNA glycosylase 2; NUDT1, nudix hydrolase 1; XRCC6, X-ray repair cross complementing 6; XRCC5, XRCC5, X-ray repair cross complementing 5; DNA-PKcs, DNA-dependent protein kinase catalytic subunit; FANCD2, fanconi anemia complementation group D2; NBN, nibrin; ERCC1, excision repair cross-complementation group 1; XPA, xeroderma pigmentosum, complementation group A; XPC, xeroderma pigmentosum, complementation group C; POLI, DNA polymerase iota; i, inhibitor; ATRi, ataxia telangiectasia and Rad3-related kinase inhibitor ; ATMi, ataxia telangiectasia mutated kinase inhibitor ATM serine/threonine kinase inhibitor; DNA-PKi, DNA-dependent protein kinase inhibitor; POLE, DNA polymerase epsilon; ARID1a, AT-rich interaction domain 1A; EZH2i, enhancer of zeste homolog 2 inhibitor; PARPi, poly(ADP-ribose) polymerase inhibitor; CHEK1/2i, checkpoint kinase 1/2 inhibitor; chemo, chemotherapy; RT, radiotherapy; HDACi, histone deacetylase inhibitor