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Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 9714

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Special Issue Editor

Prof. Dr. Rita Rezzani

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Anatomy and Physiopathology Division, Department of Clinical and Experimental Sciences, University of Brescia, 25123 Brescia, Italy
Interests: antioxidants; sex differences; skin; melatonin; oxidative stress and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence of cancer, a leading cause of death, is constantly increasing.

As we develop a better understanding of the molecular complexity underlying carcinogenesis, interventions can be established for specific mechanisms.

Despite this complexity, scientific breakthroughs have led to the discovery of the various ways in which a cell can undergo tumor transformation. Eukaryotic cells mainly depend on the consumption of oxygen, and many of their activities are related to a balance among reactive oxygen intermediates and nitrogen species. The increase in oxidative stress, if not adequately compensated for by an antioxidant defense, has a significant impact on quality of life, inducing many inflammatory processes linked to DNA mutation and tumor development.

Proper therapeutic intervention requires a good knowledge of carcinogenesis. Melatonin has demonstrated its role in the modulation of carcinogenesis, but its mechanisms remain obscure.

This Special Issue will highlight oxidative stress and cancer, covering both basic and more (pre)clinical aspects needed to improve therapies.

Prof. Dr. Rita Rezzani
Guest Editor

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Keywords

oxidative
stress
antioxidant
melatonin
carcinogenesis

Published Papers (5 papers)

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Research

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15 pages, 8744 KiB

Open AccessArticle

Melatonin Modulates the SIRT1-Related Pathways via Transdermal Cryopass-Laser Administration in Prostate Tumor Xenograft

by Francesca Bonomini, Gaia Favero, Anna Petroni, Rita Paroni and Rita Rezzani

Cancers 2023, 15(20), 4908; https://doi.org/10.3390/cancers15204908 - 10 Oct 2023

Viewed by 894

Abstract

Melatonin displays antitumor activity in several types of malignancies; however, the best delivery route and the underlying mechanisms are still unclear. Alternative non-invasive delivery route based on transdermal administration of melatonin by cryopass-laser treatment demonstrated efficiency in reducing the progression of LNCaP prostate tumor cells xenografted into nude mice by impairing the biochemical pathways affecting redox balance. Here, we investigated the impact of transdermal melatonin on the tumor dimension, microenvironment structure, and SIRT1-modulated pathways. Two groups (vehicle cryopass-laser and melatonin cryopass-laser) were treated for 6 weeks (3 treatments per week), and the tumors collected were analyzed for hematoxylin eosin staining, sirius red, and SIRT1 modulated proteins such as PGC-1α, PPARγ, and NFkB. Melatonin in addition to simple laser treatment was able to boost the antitumor cancer activity impairing the tumor microenvironment, increasing the collagen structure around the tumor, and modulating the altered SIRT1 pathways. Transdermal application is effective, safe, and feasible in humans as well, and the significance of these findings necessitates further studies on the antitumor mechanisms exerted by melatonin. Full article

(This article belongs to the Special Issue Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies)

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15 pages, 1898 KiB

Open AccessCommunication

A Lower Serum Antioxidant Capacity as a Distinctive Feature for Women with HER2+ Breast Cancer: A Preliminary Study

by Letícia L. D. Santos, Alinne T. F. Silva, Izabella C. C. Ferreira, Adriele V. Souza, Allisson B. Justino, Donizeti W. Santos, Luiz Ricardo Goulart, Carlos Eduardo Paiva, Foued S. Espíndola and Yara C. P. Maia

Cancers 2022, 14(23), 5973; https://doi.org/10.3390/cancers14235973 - 02 Dec 2022

Cited by 1 | Viewed by 1858

Abstract

The overexpression of HER2 in breast cancer (BC) can contribute to redox imbalance, which is related to damage and structural modification in many biomolecules. To the best of our knowledge, this is the first study that has investigated the infrared spectrum wavenumbers obtained by ATR-FTIR and their relationship with the levels of redox status markers such as reduced glutathione, superoxide dismutase (SOD), catalase, Ferric Reducing Antioxidant Power (FRAP), and protein carbonyl among women with HER2+ BC, HER2− BC, and benign breast disease (BBD). The study was conducted with 25 women, 17 of whom were diagnosed with BC (6 HER2+ and 11 HER2−) and 8 with BBD. Our results indicate HER2+ BC cases could be distinguished from HER2− BC and BBD cases by their serum’s antioxidant capacity [HER2+ BC vs. HER2− BC (AUC = 0.818; specificity = 81.82%; sensitivity = 66.67%); HER2+ BC vs. BBD (AUC = 0.875; specificity = 75%; sensitivity = 83.33%)]. The changes in biochemical terms that occur in serum as a result of the scarcity of antioxidants are related to a peculiar fingerprint in the infrared spectrum obtained by ATR-FTIR. In the serum of women with BBD, the SOD enzyme level is the highest, and this characteristic allowed us to distinguish them from HER2− BC. Finally, data regarding the serological antioxidant capacity of FRAP and the infrared spectrum by ATR-FTIR will allow us to assess biochemical changes that occur before clinical signs, indicating whether changes in therapy or interventions are necessary. Full article

(This article belongs to the Special Issue Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies)

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19 pages, 2527 KiB

Open AccessArticle

Elaiophylin Inhibits Tumorigenesis of Human Lung Adenocarcinoma by Inhibiting Mitophagy via Suppression of SIRT1/Nrf2 Signaling

by Jiali Ji, Ke Wang, Xinmin Meng, Hongqin Zhong, Xiyue Li, Hongqing Zhao, Guijuan Xie, Yunying Xie, Xun Wang and Xue Zhu

Cancers 2022, 14(23), 5812; https://doi.org/10.3390/cancers14235812 - 25 Nov 2022

Cited by 2 | Viewed by 1506

Abstract

Lung adenocarcinoma (LADC), the most common type of lung cancer, is still one of the most aggressive and rapidly fatal tumor types, even though achievements in new therapeutic approaches have been developed. Elaiophylin as a C2 symmetrically glycosylated 16 macrolides has been reported to be a late-stage autophagy inhibitor with a potent anti-tumor effect on various cancers. This study investigated the anti-tumor effect of elaiophylin on human LADC for the first time in in vitro and in vivo models. The in vitro study in LADC A549 cells showed that elaiophylin significantly inhibited cell viability and induced cell apoptosis through the suppression of mitophagy and induction of cellular and mitochondrial oxidative stress. Proteomic analysis and molecular docking assay implicated that SIRT1 was likely the direct target of elaiophylin in A549 cells. Further mechanistic study verified that elaiophylin reduced Nrf2 deacetylation, expression, and transcriptional activity as well as cytoplasm translocation by downregulating SIRT1 expression and deacetylase activity. Additionally, SIRT1/Nrf2 activation could attenuate elaiophylin-induced mitophagy inhibition and oxidative stress. The in vivo study in the A549-xenograft mice model showed that the anti-tumor effect of elaiophylin was accompanied by the decreased expressions of SIRT1, Nrf2, Parkin, and PINK1. Thus, the present study reports that elaiophylin has potent anti-tumor properties in LADC, which effect is likely mediated through suppressing the SIRT1/Nrf2 signaling. In conclusion, elaiophylin may be a novel drug candidate for LADC and SIRT1 may be a new therapeutic target for such devastating malignancy. Full article

(This article belongs to the Special Issue Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies)

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Review

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18 pages, 759 KiB

Open AccessReview

Oxidative Stress in Melanoma: Beneficial Antioxidant and Pro-Oxidant Therapeutic Strategies

by Alyssa L. Becker and Arup K. Indra

Cancers 2023, 15(11), 3038; https://doi.org/10.3390/cancers15113038 - 02 Jun 2023

Cited by 3 | Viewed by 2116

Abstract

Cutaneous melanoma ranks as the fifth most common cancer in the United States and represents one of the deadliest forms of skin cancer. While recent advances in systemic targeted therapies and immunotherapies have positively impacted melanoma survival, the survival rate of stage IV melanoma remains at a meager 32%. Unfortunately, tumor resistance can impede the effectiveness of these treatments. Oxidative stress is a pivotal player in all stages of melanoma progression, with a somewhat paradoxical function that promotes tumor initiation but hinders vertical growth and metastasis in later disease. As melanoma progresses, it employs adaptive mechanisms to lessen oxidative stress in the tumor environment. Redox metabolic rewiring has been implicated in acquired resistance to BRAF/MEK inhibitors. A promising approach to enhance the response to therapy involves boosting intracellular ROS production using active biomolecules or targeting enzymes that regulate oxidative stress. The complex interplay between oxidative stress, redox homeostasis, and melanomagenesis can also be leveraged in a preventive context. The purpose of this review is to provide an overview of oxidative stress in melanoma, and how the antioxidant system may be manipulated in a therapeutic context for improved efficacy and survival. Full article

(This article belongs to the Special Issue Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies)

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20 pages, 2132 KiB

Open AccessReview

Noncoding RNAs Controlling Oxidative Stress in Cancer

by Paul Holvoet

Cancers 2023, 15(4), 1155; https://doi.org/10.3390/cancers15041155 - 10 Feb 2023

Cited by 1 | Viewed by 1735

Abstract

Mitochondria in cancer cells tend to overproduce reactive oxygen species (ROS), inducing a vicious cycle between mitochondria, ROS, genomic instability, and cancer development. The first part of this review deals with the role of noncoding RNAs in regulating mitochondrial ROS production and the expression of antioxidants in cancer cells, preventing the increase of ROS in the tumor microenvironment. In addition, cytotoxic T and natural killer cells release high levels of ROS, inducing cell death, while anti-immune regulatory T cells, tumor-associated M2 macrophages, and myeloid-derived suppressor cells, at least at the initial stage of tumor growth, release low levels of ROS supporting tumor growth. Therefore, this review’s second part deals with noncoding RNAs’ role in regulating the metabolic reprogramming of immune cells about ROS release. Furthermore, the enrichment of noncoding RNAs in microvesicles allows communication between cell types in a tumor and between a tumor and tumor-adjacent tissues. Therefore, the third part illustrates how noncoding RNA-containing microvesicles secreted by mesenchymal stem cells and primary tumor cells may primarily aid the shift of immune cells to a pro-oncogenic phenotype. Conversely, microvesicles released by tumor-adjacent tissues may have the opposite effect. Our review reveals that a specific noncoding RNA may affect oxidative stress by several mechanisms, which may have opposite effects on tumor growth. Furthermore, they may be involved in mechanisms other than regulating oxidative stress, which may level out their effects on oxidative stress and tumor growth. In addition, several noncoding RNAs might share a specific function, making it very unlikely that intervening with only one of these noncoding RNAs will block this particular mechanism. Overall, further validation of the interaction between noncoding RNAs about cancer types and stages of tumor development is warranted. Full article

(This article belongs to the Special Issue Oxidative Stress and Cancer: Possible Beneficial and Antioxidant Strategies)

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