Antioxidants to Overcome Resistance in Cancer Therapy

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 July 2024 | Viewed by 434

Special Issue Editor

Special Issue Information

Dear Colleagues,

Various cancer types, including gastric, colorectal, lung, ovary, and breast cancer, are among the leading causes of death worldwide. The tumor therapeutic strategy has reduced mortality and recurrence; however, the reasons for acquired resistance are still unclear. Multifaced mechanisms like drug resistance, radioresistance, hypoxia, and growth factor deprivation are associated with a number of genes and signaling pathways that process the proliferation and death of cells. Reasons for resistance include autophagy, ER stress, DNA damage, endocytosis, oxidants, epithelial–mesenchyme transition, epigenetic modification, pathway activation, cancer-related fibroblasts, the extracellular matrix (ECM), exosomes, inflammatory immune cells, and so on. To overcome diverse chemoresistance, the relationship between antioxidants and resistant cancer models is important in the study of the mechanisms for tumor survival and cell death. Novel or candidate antioxidants against various resistant cancer models represent a new advanced strategy to overcome resistance to cancer therapy, but the underlying mechanisms are not fully clarified. This Special Issue of Antioxidants, “New antioxidants to overcome resistance in cancer therapy”, will focus on new advanced therapeutic strategies to overcome chemoresistance in various resistant cancer models. Moreover, we will encourage progress in the understanding of various resistance cancer types and focus on therapeutic approaches to develop and study new antioxidants to overcome chemoresistance.

Dr. Tae Woo Kim
Guest Editor

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Keywords

  • ROS
  • ER stress
  • NOX
  • apoptosis
  • cell death
  • natural products
  • phytochemicals
  • plant antioxidants
  • cancer
  • drug resistance

Published Papers (1 paper)

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Research

19 pages, 11957 KiB  
Article
Modeling Melanoma Heterogeneity In Vitro: Redox, Resistance and Pigmentation Profiles
by Larissa Anastacio da Costa Carvalho, Isabella Harumi Yonehara Noma, Adriana Hiromi Uehara, Ádamo Davi Diógenes Siena, Luciana Harumi Osaki, Mateus Prates Mori, Nadja Cristhina de Souza Pinto, Vanessa Morais Freitas, Wilson Araújo Silva Junior, Keiran S. M. Smalley and Silvya Stuchi Maria-Engler
Antioxidants 2024, 13(5), 555; https://doi.org/10.3390/antiox13050555 - 30 Apr 2024
Viewed by 223
Abstract
Microenvironment and transcriptional plasticity generate subpopulations within the tumor, and the use of BRAF inhibitors (BRAFis) contributes to the rise and selection of resistant clones. We stochastically isolated subpopulations (C1, C2, and C3) from naïve melanoma and found that the clones demonstrated distinct [...] Read more.
Microenvironment and transcriptional plasticity generate subpopulations within the tumor, and the use of BRAF inhibitors (BRAFis) contributes to the rise and selection of resistant clones. We stochastically isolated subpopulations (C1, C2, and C3) from naïve melanoma and found that the clones demonstrated distinct morphology, phenotypic, and functional profiles: C1 was less proliferative, more migratory and invasive, less sensitive to BRAFis, less dependent on OXPHOS, more sensitive to oxidative stress, and less pigmented; C2 was more proliferative, less migratory and invasive, more sensitive to BRAFis, less sensitive to oxidative stress, and more pigmented; and C3 was less proliferative, more migratory and invasive, less sensitive to BRAFis, more dependent on OXPHOS, more sensitive to oxidative stress, and more pigmented. Hydrogen peroxide plays a central role in oxidative stress and cell signaling, and PRDXs are one of its main consumers. The intrinsically resistant C1 and C3 clones had lower MITF, PGC-1α, and PRDX1 expression, while C1 had higher AXL and decreased pigmentation markers, linking PRDX1 to clonal heterogeneity and resistance. PRDX2 is depleted in acquired BRAFi-resistant cells and acts as a redox sensor. Our results illustrate that decreased pigmentation markers are related to therapy resistance and decreased antioxidant defense. Full article
(This article belongs to the Special Issue Antioxidants to Overcome Resistance in Cancer Therapy)
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