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Antioxidants
Special Issues
Antioxidants to Overcome Resistance in Cancer Therapy
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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: closed (20 July 2024) | Viewed by 4567

Special Issue Editor

Dr. Tae Woo Kim

E-Mail Website
Guest Editor
Department of Biopharmaceutical Engineering, Dongguk University WISE, Gyeongju 38066, Republic of Korea
Interests: ROS; calcium; ER stress; NOX; apoptosis; cell death; natural products; phytochemicals; plant antioxidants; cancer
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (2 papers)

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Research

23 pages, 5481 KiB  
Article
Synergistic Dual Targeting of Thioredoxin and Glutathione Systems Irrespective of p53 in Glioblastoma Stem Cells
by Fatemeh Jamali, Katherine Lan, Paul Daniel, Kevin Petrecca, Siham Sabri and Bassam Abdulkarim
Antioxidants 2024, 13(10), 1201; https://doi.org/10.3390/antiox13101201 - 3 Oct 2024
Cited by 2 | Viewed by 1781
Abstract
Glioblastoma (GBM) is an incurable primary brain cancer characterized by increased reactive oxygen species (ROS) production. The redox-sensitive tumor suppressor gene TP53, wild-type (wt) for 70% of patients, regulates redox homeostasis. Glioblastoma stem cells (GSCs) increase thioredoxin (Trx) and glutathione (GSH) antioxidant [...] Read more.
Glioblastoma (GBM) is an incurable primary brain cancer characterized by increased reactive oxygen species (ROS) production. The redox-sensitive tumor suppressor gene TP53, wild-type (wt) for 70% of patients, regulates redox homeostasis. Glioblastoma stem cells (GSCs) increase thioredoxin (Trx) and glutathione (GSH) antioxidant systems as survival redox-adaptive mechanisms to maintain ROS below the cytotoxic threshold. Auranofin, an FDA-approved anti-rheumatoid drug, inhibits thioredoxin reductase 1 (TrxR1). L-buthionine sulfoximine (L-BSO) and the natural product piperlongumine (PPL) inhibit the GSH system. We evaluated the cytotoxic effects of Auranofin alone and in combination with L-BSO or PPL in GBM cell lines and GSCs with a known TP53 status. The Cancer Genome Atlas/GBM analysis revealed a significant positive correlation between wtp53 and TrxR1 expression in GBM. Auranofin induced ROS-dependent cytotoxicity within a micromolar range in GSCs. Auranofin decreased TrxR1 expression, AKT (Ser-473) phosphorylation, and increased p53, p21, and PARP-1 apoptotic cleavage in wtp53-GSCs, while mutant-p53 was decreased in a mutant-p53 GSC line. Additionally, p53-knockdown in a wtp53-GSC line decreased TrxR1 expression and significantly increased sensitivity to Auranofin, suggesting the role of wtp53 as a negative redox-sensitive mechanism in response to Auranofin in GSCs. The combination of Auranofin and L-BSO synergistically increased ROS, decreased IC50s, and induced long-term cytotoxicity irrespective of p53 in GBM cell lines and GSCs. Intriguingly, Auranofin increased the expression of glutathione S-transferase pi-1 (GSTP-1), a target of PPL. Combining Auranofin with PPL synergistically decreased IC50s to a nanomolar range in GSCs, supporting the potential to repurpose Auranofin and PPL in GBM. Full article
(This article belongs to the Special Issue Antioxidants to Overcome Resistance in Cancer Therapy)
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19 pages, 10145 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
Cited by 4 | Viewed by 2249
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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