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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

24 pages, 10793 KiB

Open AccessArticle

Glutathione Reductase Expression and Its Prognostic Significance in Colon Cancer

by Marlena Brzozowa-Zasada, Adam Piecuch, Karolina Bajdak-Rusinek, Marek Michalski, Olesya Klymenko, Natalia Matysiak, Kamil Janelt and Zenon Czuba

Int. J. Mol. Sci. 2024, 25(2), 1097; https://doi.org/10.3390/ijms25021097 - 16 Jan 2024

Viewed by 833

Abstract

Maintaining a balanced redox state within cells is crucial for the sustenance of life. The process involves continuous cytosolic disulfide reduction reactions to restore oxidized proteins to their reduced thiol forms. There are two main cellular antioxidant pathways—the thioredoxin (Trx) and glutathione (GSH)/glutaredoxin (Grx) systems. In the GSH/Grx system, glutathione reductase (GR; GSR) catalyses the reduction of GSH disulfide (GSSG) to its sulfhydryl form (GSH), which can then further reduce oxidized Grxs. GR is an essential enzyme that helps in maintaining the supply of reduced glutathione-GSH, which is a significant reducing thiol found in most cells and known for its antioxidant properties. Therefore, it can have a significant impact on cancer development. To investigate this further, we performed an immunohistochemical analysis of GR protein expression in colon adenocarcinoma samples collected from patients with primary colon adenocarcinoma (stage I and II) and patients with metastasis to regional lymph nodes (stage III). The results of our study revealed a significant relationship between the immunohistochemical expression of GR and tumour histological grade, depth of invasion, regional lymph node involvement, staging, and PCNA immunohistochemical expression. It was found that 95% of patients with stage I had low levels of GR expression, whereas 89% of patients with stage III had high levels of immunohistochemical expression. A high level of expression was also detected in the patients with stage II of the disease, where almost 63% were characterized by a high expression of GR. The Western blot method revealed that the highest level of expression was found in the LS 174T cell line, which corresponds to stage II. The results of our study indicate that the immunohistochemical expression of GR may act as an independent prognostic factor associated with colon adenocarcinoma patients’ prognosis. Full article

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

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16 pages, 5093 KiB

Open AccessArticle

Glucose Deprivation Induces Cancer Cell Death through Failure of ROS Regulation

by Mingyu Kang, Joon H. Kang, In A. Sim, Do Y. Seong, Suji Han, Hyonchol Jang, Ho Lee, Sang W. Kang and Soo-Youl Kim

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

Cited by 6 | Viewed by 4194

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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