scholarly journals Glucose deprivation increases nuclear DNA repair protein Ku and resistance to radiation induced oxidative stress in human cancer cells

2009 ◽  
Vol 27 (2) ◽  
pp. 93-101 ◽  
Author(s):  
Jie Li ◽  
Roashan Ayene ◽  
Kathleen M. Ward ◽  
Eswarkumar Dayanandam ◽  
Iraimoudi S. Ayene
Keyword(s):  
Oxidative Stress ◽  
Dna Repair ◽  
Cancer Cells ◽  
Nuclear Dna ◽  
Human Cancer ◽  
Glucose Deprivation ◽  
Human Cancer Cells ◽  
Repair Protein ◽  
Dna Repair Protein ◽  
Radiation Induced

scholarly journals Bovine serum amine oxidase and spm potentiate docetaxel and interferon-α effects in inducing apoptosis on human cancer cells through the generation of oxidative stress

2008 ◽  
Vol 1783 (12) ◽  
pp. 2269-2278 ◽  
Author(s):  
M. Marra ◽  
A. Lombardi ◽  
E. Agostinelli ◽  
G. Giuberti ◽  
S. Zappavigna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Bovine Serum ◽  
Amine Oxidase ◽  
Human Cancer ◽  
Interferon Α ◽  
Human Cancer Cells

scholarly journals Telomerase-Dependent Oncolytic Adenovirus Sensitizes Human Cancer Cells to Ionizing Radiation via Inhibition of DNA Repair Machinery

2010 ◽  
Vol 70 (22) ◽  
pp. 9339-9348 ◽  
Author(s):  
Shinji Kuroda ◽  
Toshiya Fujiwara ◽  
Yasuhiro Shirakawa ◽  
Yasumoto Yamasaki ◽  
Shuya Yano ◽  
...  
Keyword(s):  
Dna Repair ◽  
Ionizing Radiation ◽  
Cancer Cells ◽  
Human Cancer ◽  
Oncolytic Adenovirus ◽  
Human Cancer Cells

scholarly journals Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation

2009 ◽  
Vol 418 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Nùkhet Aykin-Burns ◽  
Iman M. Ahmad ◽  
Yueming Zhu ◽  
Larry W. Oberley ◽  
Douglas R. Spitz
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Human Cancer ◽  
Differential Susceptibility ◽  
Glucose Deprivation ◽  
Human Colon ◽  
Normal Cells ◽  
Ht29 Cells ◽  
And Oxidative Stress

Cancer cells, relative to normal cells, demonstrate increased sensitivity to glucose-deprivation-induced cytotoxicity. To determine whether oxidative stress mediated by O2•− and hydroperoxides contributed to the differential susceptibility of human epithelial cancer cells to glucose deprivation, the oxidation of DHE (dihydroethidine; for O2•−) and CDCFH2 [5- (and 6-)carboxy-2′,7′-dichlorodihydrofluorescein diacetate; for hydroperoxides] was measured in human colon and breast cancer cells (HT29, HCT116, SW480 and MB231) and compared with that in normal human cells [FHC cells, 33Co cells and HMECs (human mammary epithelial cells)]. Cancer cells showed significant increases in DHE (2–20-fold) and CDCFH2 (1.8–10-fold) oxidation, relative to normal cells, that were more pronounced in the presence of the mitochondrial electron-transport-chain blocker, antimycin A. Furthermore, HCT116 and MB231 cells were more susceptible to glucose-deprivation-induced cytotoxicity and oxidative stress, relative to 33Co cells and HMECs. HT29 cells were also more susceptible to 2DG (2-deoxyglucose)-induced cytotoxicity, relative to FHC cells. Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. These results show that cancer cells (relative to normal cells) demonstrate increased steady-state levels of ROS (reactive oxygen species; i.e. O2•− and H2O2) that contribute to differential susceptibility to glucose-deprivation-induced cytotoxicity and oxidative stress. These studies support the hypotheses that cancer cells increase glucose metabolism to compensate for excess metabolic production of ROS and that inhibition of glucose and hydroperoxide metabolism may provide a biochemical target for selectively enhancing cytotoxicity and oxidative stress in human cancer cells.

scholarly journals Mitochondrial and H2O2Mediate Glucose Deprivation-induced Stress in Human Cancer Cells

2004 ◽  
Vol 280 (6) ◽  
pp. 4254-4263 ◽  
Author(s):  
Iman M. Ahmad ◽  
Nukhet Aykin-Burns ◽  
Julia E. Sim ◽  
Susan A. Walsh ◽  
Ryuji Higashikubo ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Glucose Deprivation ◽  
Human Cancer Cells ◽  
Induced Stress

scholarly journals Exosome component 1 cleaves single-stranded DNA and sensitizes kidney renal clear cell carcinoma cells to poly(ADP-ribose) polymerase inhibitor

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Qiaoling Liu ◽  
Qi Xiao ◽  
Zhen Sun ◽  
Bo Wang ◽  
Lina Wang ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cancer Cells ◽  
Therapeutic Strategy ◽  
Clear Cell ◽  
Clear Cell Carcinoma ◽  
Human Cancer ◽  
Renal Clear Cell Carcinoma ◽  
Dna Damages ◽  
Human Cancer Cells ◽  
Polymerase Inhibitor

Targeting DNA repair pathway offers an important therapeutic strategy for Homo sapiens (human) cancers. However, the failure of DNA repair inhibitors to markedly benefit patients necessitates the development of new strategies. Here, we show that exosome component 1 (EXOSC1) promotes DNA damages and sensitizes human kidney renal clear cell carcinoma (KIRC) cells to DNA repair inhibitor. Considering that endogenous source of mutation (ESM) constantly assaults genomic DNA and likely sensitize human cancer cells to the inhibitor, we first analyzed the statistical relationship between the expression of individual genes and the mutations for KIRC. Among the candidates, EXOSC1 most notably promoted DNA damages and subsequent mutations via preferentially cleaving C site(s) in single-stranded DNA. Consistently, EXOSC1 was more significantly correlated with C>A transversions in coding strands than these in template strands in human KIRC. Notably, KIRC patients with high EXOSC1 showed a poor prognosis, and EXOSC1 sensitized human cancer cells to poly(ADP-ribose) polymerase inhibitor. These results show that EXOSC1 acts as an ESM in KIRC, and targeting EXOSC1 might be a potential therapeutic strategy.

scholarly journals dUTPase inhibition confers susceptibility to a thymidylate synthase inhibitor in DNA‐repair‐defective human cancer cells

2020 ◽  
Vol 112 (1) ◽  
pp. 422-432
Author(s):  
Tatsushi Yokogawa ◽  
Wakako Yano ◽  
Sayaka Tsukioka ◽  
Akiko Osada ◽  
Takeshi Wakasa ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cancer Cells ◽  
Thymidylate Synthase ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Thymidylate Synthase Inhibitor ◽  
Synthase Inhibitor

Abstract 265: Assessment Of Oxidative DNA Double Strand Break And Repair In Cardiomyocytes

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Bo Ye ◽  
Ning Hou ◽  
Lu Xiao ◽  
Haodong Xu ◽  
Faqian Li
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Dna Repair ◽  
Stress Responses ◽  
Strand Break ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Repair Protein ◽  
Dna Repair Protein

Backgrounds: DNA damage occurs in cardiomyocytes during normal cellular metabolism and is significantly increased under cardiac stresses. How cardiomyocytes repair their DNA damage, especially DNA double strand breaks (DSBs), remains undetermined. We assessed DSBs caused by oxidative stress. More importantly, we investigated the spatiotemporal dynamics of DNA repair protein assembly/disassembly in DNA damage sites. Methods: Cultured neonatal rat cardiomyocytes were treated with different doses of hydrogen peroxide (H2O2) for 30 minutes to assess DNA damage response (DDR). To investigate the dynamics of DDR, cells were treated with 200 uM H2O2 and followed up to 72 hours. DSBs were evaluated by counting DNA damage foci after staining with antibody against histone H2AX phosphorylation at serine 139 (g-H2AX). The dynamics and posttranslational modification of DNA repair proteins were determined by Western blotting, immunolabeling, and confocal microscopy. Result: g-H2AX was proportionally increased to H2O2 dosage. Discrete nuclear g-H2AX foci were seen 30 minutes after hydrogen peroxide treatment with 50 uM, but became pannuclear when H2O2 was above 400 uM. At 200 uM of hydrogen peroxide, g-H2AX started to increase at 15 minutes and reached to highest levels at 60 minutes with up to 70 nuclear foci, started to decline at 2 hours, and returned to basal levels at 24 hours. DDR transducer kinase, ataxia telangiectasia mutated (ATM) was activated at 5 minutes with increased phosphorylation at serine 1981 (pATM) which started to decrease at 24 hours, but remained elevated up to 48 hours. Another DDR transducer kinase, ATM and Rad3-related (ATR) showed a biphasic activation at 30 minutes and 8 hours. ATM and ATR colocalized with g-H2AX. DNA damage mediator proteins such as MRN complex and p53BP1 were also recruited to sites of DNA damage at g-H2AX foci. Conclusions: DSBs and their repair have emerged as a new frontier of stress responses. Newly developed methods for studying g-H2AX and DNA repair protein dynamics can be explored to investigate DDR to oxidative stress in cardiomyocytes.

Silk sericin induced pro-oxidative stress leads to apoptosis in human cancer cells

2019 ◽  
Vol 123 ◽  
pp. 275-287 ◽  
Author(s):  
Jadi Praveen Kumar ◽  
Biman B. Mandal
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Human Cancer ◽  
Silk Sericin ◽  
Human Cancer Cells

scholarly journals Disruption of telomere equilibrium sensitises human cancer cells to DNA repair inhibition and radiation

2016 ◽  
Vol 118 ◽  
pp. S49
Author(s):  
S. Venkatesan ◽  
R. Lal Gurung ◽  
S. Sameni ◽  
S. Sethu ◽  
M.P. Hande
Keyword(s):  
Dna Repair ◽  
Cancer Cells ◽  
Human Cancer ◽  
Human Cancer Cells
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