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Special Issue "New Players in the Research of Oxidative Stress and Cancer"

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Dear Colleagues,

In spite of the huge improvement in cancer diagnostics and treatment it is still a great challenge to provide good predicitve markers and therapy to diaganose, predict the outcome and to cure the disease without recurrence. Oxidative stress is one of the factors which plays a role in bot cancer development but also as a mechanism of action against it. Therefore, it is not surprising that new players are discovered with a role in oxidative stress modulation and cancer development and progression. The issue is open to original and review papers describing new player in oxidative stress responce in cancer, as well as antioxidative defence that can be used in cancer diagnostics, prediction of the disease outcome and possible new therapeutical targets.

Dr. Ana Čipak Gašparović
Guest Editor

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Keywords

cancer
oxidative stress
biomarkes
redox signaling pathway
therapy resistance

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Research

Open AccessArticle

Glucose Deprivation Induces Cancer Cell Death through Failure of ROS Regulation

and

Int. J. Mol. Sci. 2023, 24(15), 11969; https://doi.org/10.3390/ijms241511969 - 26 Jul 2023

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Abstract

In previous work, we showed that cancer cells do not depend on glycolysis for ATP production, but they do on fatty acid oxidation. However, we found some cancer cells induced cell death after glucose deprivation along with a decrease of ATP production. We investigated the different response of glucose deprivation with two types of cancer cells including glucose insensitive cancer cells (GIC) which do not change ATP levels, and glucose sensitive cancer cells (GSC) which decrease ATP production in 24 h. Glucose deprivation-induced cell death in GSC by more than twofold after 12 h and by up to tenfold after 24 h accompanied by decreased ATP production to compare to the control (cultured in glucose). Glucose deprivation decreased the levels of metabolic intermediates of the pentose phosphate pathway (PPP) and the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) in both GSC and GIC. However, glucose deprivation increased reactive oxygen species (ROS) only in GSC, suggesting that GIC have a higher tolerance for decreased NADPH than GSC. The twofold higher ratio of reduced/oxidized glutathione (GSH/GSSG) in GIS than in GSC correlates closely with the twofold lower ROS levels under glucose starvation conditions. Treatment with N-acetylcysteine (NAC) as a precursor to the biologic antioxidant glutathione restored ATP production by 70% and reversed cell death caused by glucose deprivation in GSC. The present findings suggest that glucose deprivation-induced cancer cell death is not caused by decreased ATP levels, but rather triggered by a failure of ROS regulation by the antioxidant system. Conclusion is clear that glucose deprivation-induced cell death is independent from ATP depletion-induced cell death. Full article

(This article belongs to the Special Issue New Players in the Research of Oxidative Stress and Cancer)

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Special Issue "New Players in the Research of Oxidative Stress and Cancer"

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