Total Flavonoids Isolated from Diospyros kaki L. f. Leaves Induced Apoptosis and Oxidative Stress in Human Cancer Cells

2020 ◽  
Vol 40 (9) ◽  
pp. 5201-5210
Author(s):  
LI CHEN ◽  
YUHANG GUO ◽  
GHEDA ALSAIF ◽  
YING GAO
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Human Cancer ◽  
Diospyros Kaki ◽  
Total Flavonoids ◽  
Human Cancer Cells ◽  
Induced Apoptosis ◽  
And Oxidative Stress

p53 acetylation enhances Taxol-induced apoptosis in human cancer cells

APOPTOSIS ◽  
2012 ◽  
Vol 18 (1) ◽  
pp. 110-120 ◽  
Author(s):  
Jae Hyeong Kim ◽  
Eun-Kyung Yoon ◽  
Hye-Jin Chung ◽  
Seong-Yeol Park ◽  
Kyeong-Man Hong ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Induced Apoptosis

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.

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