UmorsTable 1 Overview of HiF-1-mediated chemo-/radioresistance mechanismsResistance phenotype DNA repair pathway activation DNA repair pathway activation DNA repair pathway activation DNA repair pathway activation DNA repair pathway activation DNA repair pathway activation Metabolic reprogramming Metabolic reprogramming Metabolic reprogramming Apoptosis 5-Fluoro-2′-deoxycytidine Data Sheet inhibition Apoptosis inhibition Apoptosis inhibition Autophagy activation Autophagy activation Autophagy activation Autophagy activation Autophagy activation Autophagy activation Molecular basis (if known) XPA DNA-PK XPA Cell model Lung cancer cells Mouse embryonic fibroblasts Germ cell tumors Hepatocellular carcinoma cells Gastric cancer cells Mouse mesenchymal stromal cells Lung cancer cells Colorectal cancer cells Various myeloma cells Colon cancer cells Gastric cancer cells Gastric cancer cells Colon cancer cells Lung cancer cells Lung cancer cells Osteosarcoma cells Lung cancer cells Mouse mesenchymal stromal cells Therapies Cisplatin etoposide Cisplatin Radiotherapy Chemo-/radiotherapy Radiotherapy Cisplatin RiP-dependent necroptosis Bortezomib Chemo-/radiotherapy 5-Fluorouracil Chemo-/radiotherapy Radiotherapy Cisplatin Radiotherapy Radiotherapy Silver nanoparticle Radiotherapy Reference 36 40 41 42 43 44 47 51 53 58 59 60 70 71 72 30 73DNA-PK, H2AX GLUT1 GLUT1 LDHA STAT3, TCF4 P53 Survivin, Bax, caspase 3/8 MiRNA20, Bcl2 BNiP3, Beclin-1 Beclin-1, c-Jun LC3ii mTOR/Pi3KAbbreviations: DNA-PK, DNA-dependent protein kinase; RiP, receptor-interacting protein.of DNA damage induced by chemo-/radiotherapy. Also, Yang et al31 reported that the hepatocarcinoma cells exhibited higher activity of DNA harm repair pathway than normal cells and Stover et al32 reported that activated DNA repair pathway can be a considerable result in of chemo-/radioresistance in tumor cells. As a result, just after exposure to chemotherapeutic drugs and radiation, many cancer cells could keep away from death by means of the activation of DNA repair pathway. Fortini et al33 reported that chemo-/radiotherapy may well induce single-stranded DNA breaks (SSBs) or doublestranded DNA breaks (DSBs), which have to be repaired or will have to commence apoptosis. The repair of SSBs is carried out by big pathways: base excision repair (BER), poly-ADPribose polymerase (PARP-1), and both XPA and XPD would be the essential molecules inside the BER method. DSBs are more harmful on cell survival than SSBs and are powerful activators of apoptosis simply because cell death might be induced by the persistence of DSBs if not repaired. To preserve genomic stability and survival, cells have developed DNA harm response (DDR) to handle DSBs in line with Fortini et al.33 Fortini et al33 also observed that cells respond to DSBs immediately and accurately, that 3 steps might be required: first, the harm have to be detected by each ataxia telangiectasia mutated (ATM) and ataxia telangiectasia RED3 associated (ATR); second, damaged proteins should match into the transmembrane proteins from the cells; and lastly, cells react to repair DSBs beneath the function of the DNAdependent protein kinase (DNA-PK) and histone H2AX,when the DNA repair is failed, Li et al34 proposed that the ATM/ATR complex activates P53, its downstream molecule, which induces apoptosis. A large variety of studies showed that HIF-1 could raise the potential of DNA damage repair by way of the regulation of DNA repair pathway, therefore leading to the chemo-/ radioresistance in tumor cells. As an example, Um et al35 identified that HIF-1 contributed to resista.