Targeting Oxidative Stress in Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (20 March 2022) | Viewed by 3347

Special Issue Editors


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Guest Editor
College of Pharmacy, Keimyung University, 1000 Sindang-dong, Dalseo-Gu, Daegu 704-701, Korea
Interests: reactive oxygen species; oxidative stress; skin cancer; carcinogenesis; cancer signlaing pathway; prostanoid receptor; apoptosis; cell proliferation
Special Issues, Collections and Topics in MDPI journals
Department of Chemistry, College of Convergence and Integrated Science, Kyonggi University, Suwon 16227, Korea
Interests: oxidative stress; cancer

Special Issue Information

Dear Colleagues,

Oxidative stress is defined as the shift of the balance between cellular oxidation and reduction potential towards the oxidizing part, provoked when cellular antioxidant defense capacity is overwhelmed by the massive production of reactive oxygen species (ROS). Excessive ROS production causes oxidative stress, which is implicated in aging and in the pathogenesis of many human disorders, including cancer, obesity, neurodegenerative diseases, and diabetes. Redox imbalance towards pro-oxidant conditions has been considered to be implicated in the pathogenesis of tumor development and progression. In addition, some cellular signaling and metabolic pathways altered due to oxidative and reductive stress have been identified as major contributors to tumorigenesis. Moreover, cancer cells are located in a very complex microenvironment together with stromal components that participate to enhance oxidative stress to promote tumor progression. Understanding the oxidative stress between surrounding cells in the tumor microenvironment can also be a very important topic. This Special Issue aims to propose a possibility for overcoming cancer by targeting oxidative stress in several aspects.

Specifically, this Issue entitled “Targeting Oxidative Stress in Cancer” solicits original research and review articles on topics including the role and contribution of oxidative stress in cancer. This Issue aims to highlight relationships between oxidative stress and tumorigenesis, as well as their role in the pathophysiology and treatment of cancer.

Dr. Kyung-Soo Chun
Dr. Do-Hee Kim
Guest Editors

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Keywords

  • oxidative stress
  • cancer
  • metabolism
  • inflammation
  • biomarkers

Published Papers (1 paper)

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Research

17 pages, 4014 KiB  
Communication
5-Azacytidine Inhibits the Activation of Senescence Program and Promotes Cytotoxic Autophagy during Trdmt1-Mediated Oxidative Stress Response in Insulinoma β-TC-6 Cells
by Kamila Filip, Anna Lewińska, Jagoda Adamczyk-Grochala, Antonella Marino Gammazza, Francesco Cappello, Marianna Lauricella and Maciej Wnuk
Cells 2022, 11(7), 1213; https://doi.org/10.3390/cells11071213 - 4 Apr 2022
Cited by 13 | Viewed by 2942
Abstract
5-Azacytidine (5-azaC), a methyltransferase inhibitor and anticancer drug, can promote several cellular stress responses such as apoptosis, autophagy, and senescence. The action of 5-azaC is complex and can be modulated by dose, time of treatment, and co-administration with oxidants. Insulinoma is a rare [...] Read more.
5-Azacytidine (5-azaC), a methyltransferase inhibitor and anticancer drug, can promote several cellular stress responses such as apoptosis, autophagy, and senescence. The action of 5-azaC is complex and can be modulated by dose, time of treatment, and co-administration with oxidants. Insulinoma is a rare pancreatic neuroendocrine tumor with limited chemotherapeutic options. In the present study, two cellular models of insulinoma were considered, namely NIT-1 and β-TC-6 mouse cells, to evaluate the effects of 5-azaC post-treatment during hydrogen peroxide-induced oxidative stress. 5-azaC attenuated the development of oxidant-induced senescent phenotype in both cell lines. No pro-apoptotic action of 5-azaC was observed in cells treated with the oxidant. On the contrary, 5-azaC stimulated an autophagic response, as demonstrated by the increase in phosphorylated eIF2α and elevated pools of autophagic marker LC3B in oxidant-treated β-TC-6 cells. Notably, autophagy resulted in increased necrotic cell death in β-TC-6 cells with higher levels of nitric oxide compared to less affected NIT-1 cells. In addition, 5-azaC increased levels of RNA methyltransferase Trdmt1, but lowered 5-mC and m6A levels, suggesting Trdmt1 inhibition. We postulate that the 5-azaC anticancer action may be potentiated during oxidative stress conditions that can be used to sensitize cancer cells, at least insulinoma cells, with limited drug responsiveness. Full article
(This article belongs to the Special Issue Targeting Oxidative Stress in Cancer)
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