UmorsTable 1 Overview of HiF-1-mediated chemo-/radioresistance mechanismsResistance phenotype DNA repair pathway activation DNA repair pathway

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 inhibition Apoptosis inhibition Apoptosis inhibition Autophagy activation Autophagy activation Autophagy activation Autophagy activation Autophagy activation Autophagy activation Molecular basis (if identified) 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 Several 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 damage repair pathway than standard cells and Stover et al32 reported that activated DNA repair pathway is a important bring about of chemo-/radioresistance in tumor cells. Thus, right after exposure to chemotherapeutic drugs and radiation, lots of cancer cells could stay clear of death through the activation of DNA repair pathway. Fortini et al33 reported that chemo-/radiotherapy may perhaps induce single-stranded DNA breaks (SSBs) or doublestranded DNA breaks (DSBs), which must be repaired or will have to commence apoptosis. The repair of SSBs is carried out by important pathways: base excision repair (BER), poly-ADPribose polymerase (PARP-1), and each XPA and XPD would be the key molecules inside the BER procedure. DSBs are more damaging on cell survival than SSBs and are strong activators of apoptosis since cell death could be induced by the persistence of DSBs if not repaired. To preserve genomic stability and survival, cells have developed DNA harm response (DDR) to manage DSBs based on Fortini et al.33 Fortini et al33 also observed that cells ��-cedrene Biological Activity respond to DSBs speedily and accurately, that 3 actions may be essential: 1st, the damage should be detected by both ataxia telangiectasia mutated (ATM) and ataxia telangiectasia RED3 related (ATR); second, broken proteins should fit in to the transmembrane proteins in the cells; and lastly, cells react to repair DSBs below the function on the DNAdependent protein kinase (DNA-PK) and histone H2AX,when the DNA repair is failed, Li et al34 proposed that the ATM/ATR complicated activates P53, its downstream molecule, which induces apoptosis. A large Cloxacillin (sodium) Purity & Documentation number of research showed that HIF-1 could boost the potential of DNA damage repair by way of the regulation of DNA repair pathway, therefore major towards the chemo-/ radioresistance in tumor cells. For example, Um et al35 identified that HIF-1 contributed to resista.