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Special Issue "Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers"

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6821

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Special Issue Editor

Dr. Meng-Er Huang

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Guest Editor

CNRS, Institut de Chimie des Substances Naturelles, UPR 2301, Université Paris-Saclay, 91198 Gif-sur-Yvette, France
Interests: oxidative stress; cancer stem cells; drug combinations; anticancer strategies

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) homeostasis and dynamic intracellular reductive/oxidative (redox) balance play a key role in cell physiology and contribute to cell fate decisions. In many cancer cells, cellular events such as activation of oncogenes, aberrant metabolic stress, and mitochondrial dysfunction can increase ROS levels, leading to intrinsic oxidative stress and a persistent pro-oxidative status. Therefore, the malignant cells are more dependent on antioxidants for cell survival and more vulnerable to further oxidative insults than their normal counterparts. It is conceivable that we could induce preferential cancer cell death by pharmacological interventions targeting the cellular redox system. This is the biological basis of oxidative stress- and redox-based anticancer strategy that could have significant therapeutic implications. Furthermore, it has been demonstrated that, at least in some cases, redox adaptation plays an important role in intrinsic or acquired resistance to chemotherapy/radiotherapy. Redox modulation to abrogate such adaptation mechanisms in combination with conventional chemotherapy or radiotherapy can also be exploited for therapeutic benefits.

This Special Issue is devoted to publishing original research articles on redox alterations and redox adaptation mechanisms in cancer cells and cancer stem cells, mechanisms of action of redox-modulating agents and drug combinations, and translational studies and clinical evaluations. Review articles on these topics are also welcome. We aim to provide a comprehensive update on oxidative stress- and redox-based therapeutic strategies in cancers.

Dr. Meng-Er Huang
Guest Editor

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Keywords

reactive oxygen species
oxidative stress
redox modulation
redox adaptation
cancer cells
cancer stem cells
drug combinations
anticancer strategies

Published Papers (4 papers)

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Research

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Open AccessArticle

The Antimalarial Drug Artesunate Mediates Selective Cytotoxicity by Upregulating HO-1 in Melanoma Cells

Finn Jochims

Rebecca Strohm

Claudia von Montfort

Chantal-Kristin Wenzel

and

Biomedicines 2023, 11(9), 2393; https://doi.org/10.3390/biomedicines11092393 - 27 Aug 2023

Viewed by 546

Abstract

Despite great efforts to develop new therapeutic strategies to combat melanoma, the prognosis remains rather poor. Artesunate (ART) is an antimalarial drug displaying anti-cancer effects in vitro and in vivo. In this in vitro study, we investigated the selectivity of ART on melanoma cells. Furthermore, we aimed to further elucidate the mechanism of the drug with a focus on the role of iron, the induction of oxidative stress and the implication of the enzyme heme oxygenase 1 (HO-1). ART treatment decreased the cell viability of A375 melanoma cells while it did not affect the viability of normal human dermal fibroblasts, used as a model for normal (healthy) cells. ART’s toxicity was shown to be dependent on intracellular iron and the drug induced high levels of oxidative stress as well as upregulation of HO-1. Melanoma cells deficient in HO-1 or treated with a HO-1 inhibitor were less sensitive towards ART. Taken together, our study demonstrates that ART induces oxidative stress resulting in the upregulation of HO-1 in melanoma cells, which subsequently triggers the effect of ART’s own toxicity. This new finding that HO-1 is involved in ART-mediated toxicity may open up new perspectives in cancer therapy. Full article

(This article belongs to the Special Issue Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers)

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Open AccessArticle

The Sesquiterpene Lactone Cynaropicrin Manifests Strong Cytotoxicity in Glioblastoma Cells U-87 MG by Induction of Oxidative Stress

Rossella Rotondo

Maria Antonietta Oliva

and

Antonietta Arcella

Biomedicines 2022, 10(7), 1583; https://doi.org/10.3390/biomedicines10071583 - 02 Jul 2022

Cited by 2 | Viewed by 1499

Abstract

Cynaropicrin has shown a wide range of pharmacological properties, such as antitumor action. Here, we showed the inhibitory effect of Cyn on human glioblastoma cell U-87 MG growth. According to the IC50 values, Cyn 4, 8 and 10 µM displayed a significant cytotoxicity, as confirmed by the cell count and MTT assay. Furthermore, Cyn completely abolished the ability of U-87 MG to form colonies and induced drastic morphological changes. Interestingly, pretreatment with ROS scavenger N-acetylcysteine 3 mM reversed the cytotoxicity induced by Cyn 25 µM and preserved the cells by morphological changes. Therefore, oxidative stress induction was evaluated at low 8- and high 25-µM concentrations in U-87 MG, as demonstrated by the quantitative and qualitative analysis of ROS. A prolonged increase in ROS generation under Cyn 25 µM exposure was followed by the loss of the mitochondrial membrane potential in treated U-87 MG cells. An acute treatment with Cyn 25 µM induced Cyt c release, as revealed by immunofluorescence staining and the activation of cell death pathways, apoptosis and autophagy. On the other hand, chronic treatment with Cyn 8 µM induced senescence, as revealed by the increase in SA-β-Gal activity. Moreover, at this concentration, Cyn led to ERK dephosphorylation accompanied by a relevant reduction of the NF-κB p65 subunit. Finally, the combined effect of TMZ and Cyn resulted in synergistic cytotoxicity, as evaluated by the Bliss additivity model. The strong cytotoxicity of Cyn was also confirmed on IDH1 mutant U-87 MG cells and patient-derived IDH wild-type glioblastoma cell lines NULU and ZAR. In conclusion, given the high toxicity at minimal concentrations, the high inhibition of tumor cell growth and synergy with the standard drug for glioblastoma TMZ, Cyn could be proposed as a potential adjuvant for the treatment of glioblastoma. Full article

(This article belongs to the Special Issue Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers)

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Review

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Redox-Regulation in Cancer Stem Cells

Uwe Lendeckel

and

Carmen Wolke

Biomedicines 2022, 10(10), 2413; https://doi.org/10.3390/biomedicines10102413 - 27 Sep 2022

Cited by 3 | Viewed by 1365

Abstract

Cancer stem cells (CSCs) represent a small subset of slowly dividing cells with tumor-initiating ability. They can self-renew and differentiate into all the distinct cell populations within a tumor. CSCs are naturally resistant to chemotherapy or radiotherapy. CSCs, thus, can repopulate a tumor after therapy and are responsible for recurrence of disease. Stemness manifests itself through, among other things, the expression of stem cell markers, the ability to induce sphere formation and tumor growth in vivo, and resistance to chemotherapeutics and irradiation. Stemness is maintained by keeping levels of reactive oxygen species (ROS) low, which is achieved by enhanced activity of antioxidant pathways. Here, cellular sources of ROS, antioxidant pathways employed by CSCs, and underlying mechanisms to overcome resistance are discussed. Full article

(This article belongs to the Special Issue Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers)

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Open AccessReview

The Thioredoxin System of Mammalian Cells and Its Modulators

and

Biomedicines 2022, 10(7), 1757; https://doi.org/10.3390/biomedicines10071757 - 21 Jul 2022

Cited by 8 | Viewed by 2592

Abstract

Oxidative stress involves the increased production and accumulation of free radicals, peroxides, and other metabolites that are collectively termed reactive oxygen species (ROS), which are produced as by-products of aerobic respiration. ROS play a significant role in cell homeostasis through redox signaling and are capable of eliciting damage to macromolecules. Multiple antioxidant defense systems have evolved to prevent dangerous ROS accumulation in the body, with the glutathione and thioredoxin/thioredoxin reductase (Trx/TrxR) systems being the most important. The Trx/TrxR system has been used as a target to treat cancer through the thiol–disulfide exchange reaction mechanism that results in the reduction of a wide range of target proteins and the generation of oxidized Trx. The TrxR maintains reduced Trx levels using NADPH as a co-substrate; therefore, the system efficiently maintains cell homeostasis. Being a master regulator of oxidation–reduction processes, the Trx-dependent system is associated with cell proliferation and survival. Herein, we review the structure and catalytic properties of the Trx/TrxR system, its role in cellular signaling in connection with other redox systems, and the factors that modulate the Trx system. Full article

(This article belongs to the Special Issue Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers)

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Special Issue "Oxidative Stress– and Redox–Based Therapeutic Strategy in Cancers"

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