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Antioxidants
Special Issues
Oxidative Stress Induced DNA Damage in Cancer Treatment
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Oxidative Stress Induced DNA Damage in Cancer Treatment

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 April 2023) | Viewed by 7642

Special Issue Editors

Dr. Karima Ait-Aissa

E-Mail Website
Guest Editor
Internal Medicine-Cardiovascular Medicine, University of Iowa, Iowa City, IA, USA
Interests: cardiovascular physiology; FMD; TLR; radiation; mitochondrial function; DNA damage; microbiome
Special Issues, Collections and Topics in MDPI journals
Dr. Andreas Beyer

E-Mail Website1 Website2
Guest Editor
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA
Interests: coronary artery disease; mitochondria; cardio-oncology; microcirculation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Anticancer therapies involving the generation of oxidative stress have gained considerable attention in recent years. Cytosolic and mitochondrial Reactive Oxygen Species (ROS) play an important role in various cellular functions because they are involved in a number of signalling pathways; however, when their levels reach excessive amounts and can no longer be regulated or suppressed, they can cause damage to DNA and proteins, causing different organelles damages. In cancer cells, current therapies target this effect to induce cellular death and stop cancer growth. However, in healthy cells, different outcomes can be obtained. In general, repair mechanisms will be activated and the damage will be reduced; otherwise, apoptosis will be initiated, leading to cellular death. In some cases, DNA can be excessively damaged, and this can lead to the formation of cancerous cells or cellular damage. When ROS cannot be neutralised after a period of accumulation, this results in DNA damage and can contribute to tumour proliferation, survival, chronic inflammation, angiogenesis, and different organ dysfunctions.

Contributions to this Special Issue may cover all research aspects related to pathways involving ROS-induced DNA damage during chemotherapy or radiation therapy. We aim to specifically discuss cellular mechanisms that are involved in anticancer-therapy-induced DNA damage via oxidative stress pathways in both healthy and cancer cells.

Dr. Karima Ait-Aissa
Dr. Andreas Beyer
Guest Editors

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

  • Chemotherapy
  • Radiation therapy
  • DNA damage
  • Oxidative stress
  • ROS
  • Cancer resistance
  • Tumor proliferation
  • Cellular death
  • Normal tissue injury
  • Bystander effect

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Published Papers (3 papers)

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Research

24 pages, 4385 KiB  
Article
Auranofin Synergizes with the PARP Inhibitor Olaparib to Induce ROS-Mediated Cell Death in Mutant p53 Cancers
by Laurie Freire Boullosa, Jinthe Van Loenhout, Tal Flieswasser, Christophe Hermans, Céline Merlin, Ho Wa Lau, Elly Marcq, Marlies Verschuuren, Winnok H. De Vos, Filip Lardon, Evelien L. J. Smits and Christophe Deben
Antioxidants 2023, 12(3), 667; https://doi.org/10.3390/antiox12030667 - 8 Mar 2023
Cited by 9 | Viewed by 3103
Abstract
Auranofin (AF) is a potent, off-patent thioredoxin reductase (TrxR) inhibitor that efficiently targets cancer via reactive oxygen species (ROS)- and DNA damage-mediated cell death. The goal of this study is to enhance the efficacy of AF as a cancer treatment by combining it [...] Read more.
Auranofin (AF) is a potent, off-patent thioredoxin reductase (TrxR) inhibitor that efficiently targets cancer via reactive oxygen species (ROS)- and DNA damage-mediated cell death. The goal of this study is to enhance the efficacy of AF as a cancer treatment by combining it with the poly(ADP-ribose) polymerase-1 (PARP) inhibitor olaparib (referred to as ‘aurola’). Firstly, we investigated whether mutant p53 can sensitize non-small cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) cancer cells to AF and olaparib treatment in p53 knock-in and knock-out models with varying p53 protein expression levels. Secondly, we determined the therapeutic range for synergistic cytotoxicity between AF and olaparib and elucidated the underlying molecular cell death mechanisms. Lastly, we evaluated the effectiveness of the combination strategy in a murine 344SQ 3D spheroid and syngeneic in vivo lung cancer model. We demonstrated that high concentrations of AF and olaparib synergistically induced cytotoxicity in NSCLC and PDAC cell lines with low levels of mutant p53 protein that were initially more resistant to AF. The aurola combination also led to the highest accumulation of ROS, which resulted in ROS-dependent cytotoxicity of mutant p53 NSCLC cells through distinct types of cell death, including caspase-3/7-dependent apoptosis, inhibited by Z-VAD-FMK, and lipid peroxidation-dependent ferroptosis, inhibited by ferrostatin-1 and alpha-tocopherol. High concentrations of both compounds were also needed to obtain a synergistic cytotoxic effect in 3D spheroids of the murine lung adenocarcinoma cell line 344SQ, which was interestingly absent in 2D. This cell line was used in a syngeneic mouse model in which the oral administration of aurola significantly delayed the growth of mutant p53 344SQ tumors in 129S2/SvPasCrl mice, while either agent alone had no effect. In addition, RNA sequencing results revealed that AF- and aurola-treated 344SQ tumors were negatively enriched for immune-related gene sets, which is in accordance with AF’s anti-inflammatory function as an anti-rheumatic drug. Only 344SQ tumors treated with aurola showed the downregulation of genes related to the cell cycle, potentially explaining the growth inhibitory effect of aurola since no apoptosis-related gene sets were enriched. Overall, this novel combination strategy of oxidative stress induction (AF) with PARP inhibition (olaparib) could be a promising treatment for mutant p53 cancers, although high concentrations of both compounds need to be reached to obtain a substantial cytotoxic effect. Full article
(This article belongs to the Special Issue Oxidative Stress Induced DNA Damage in Cancer Treatment)
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18 pages, 6589 KiB  
Article
Methanol Extract of Clavularia inflata Exerts Apoptosis and DNA Damage to Oral Cancer Cells
by Yin-Yin Hsu, Ya-Ting Chuang, Ching-Yu Yen, Ming-Ya Cheng, Ching-Yeu Chen, Yuan-Bin Cheng and Hsueh-Wei Chang
Antioxidants 2022, 11(9), 1777; https://doi.org/10.3390/antiox11091777 - 8 Sep 2022
Cited by 2 | Viewed by 1720
Abstract
Antiproliferation effects of Clavularia-derived natural products against cancer cells have been reported on, but most studies have focused on identifying bioactive compounds, lacking a detailed investigation of the molecular mechanism. Crude extracts generally exhibit multiple targeting potentials for anticancer effects, but they [...] Read more.
Antiproliferation effects of Clavularia-derived natural products against cancer cells have been reported on, but most studies have focused on identifying bioactive compounds, lacking a detailed investigation of the molecular mechanism. Crude extracts generally exhibit multiple targeting potentials for anticancer effects, but they have rarely been assessed for methanol extracts of Clavularia inflata (MECI). This investigation aims to evaluate the antiproliferation of MECI and to examine several potential mechanisms between oral cancer and normal cells. A 24 h MTS assay demonstrated that MECI decreased cell viability in several oral cancer cell lines more than in normal cells. N-acetylcysteine (NAC), an oxidative stress inhibitor, recovered these antiproliferation effects. Higher oxidative stress was stimulated by MECI in oral cancer cells than in normal cells, as proven by examining reactive oxygen species and mitochondrial superoxide. This preferential induction of oxidative stress was partly explained by downregulating more cellular antioxidants, such as glutathione, in oral cancer cells than in normal cells. Consequently, the MECI-generated high oxidative stress in oral cancer cells was preferred to trigger more subG1 population, apoptosis expression (annexin V and caspase activation), and DNA damage, reverted by NAC. In conclusion, MECI is a potent marine natural product showing preferential antiproliferation against oral cancer cells. Full article
(This article belongs to the Special Issue Oxidative Stress Induced DNA Damage in Cancer Treatment)
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16 pages, 3759 KiB  
Article
Laminarin Attenuates ROS-Mediated Cell Migration and Invasiveness through Mitochondrial Dysfunction in Pancreatic Cancer Cells
by Woonghee Lee, Gwonhwa Song and Hyocheol Bae
Antioxidants 2022, 11(9), 1714; https://doi.org/10.3390/antiox11091714 - 30 Aug 2022
Cited by 10 | Viewed by 2280
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a notoriously aggressive type of cancer with a high metastasis rate. It is conventionally treated by surgical resection and neoadjuvant chemotherapy. However, continuous chemotherapy leads to relapse in most PDAC patients due to chemical resistance. Therefore, novel anticancer [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a notoriously aggressive type of cancer with a high metastasis rate. It is conventionally treated by surgical resection and neoadjuvant chemotherapy. However, continuous chemotherapy leads to relapse in most PDAC patients due to chemical resistance. Therefore, novel anticancer agents need to be identified and developed. The antitumor activities of laminarin extracted from brown algae against hepatocarcinoma, lung, and colon cancer have been established. However, its effects on pancreatic cancer have remained obscure. Our study identified the anticancer effects of laminarin on pancreatic cancer cells and tried to explain its intracellular mechanisms. We assessed the cell viability of PANC-1 and MIA PaCa-2 cells using MTT assay. Hanging drop method was used for the spheroid formation. Flow cytometry was conducted to evaluate the several intracellular alterations including apoptosis, ROS production, mitochondrial membrane potential (MMP), and calcium concentration induced by laminarin. An invasion test was performed to assess the inhibitory effect of laminarin on cell migration and the invasive genes were evaluated by RT-qPCR. Signaling pathway related with anticancer effects of laminarin was analyzed by western blot. We report that inhibiting laminarin increased the proliferation and viability of the representative pancreatic cancer cell lines, MIA PaCa-2 and PANC-1. Laminarin triggered apoptosis and mitochondrial impairment as evidenced by depolarized mitochondrial membranes, disrupted calcium, and suppressed cell migration caused by reactive oxygen species production and related intracellular signaling pathways. Moreover, laminarin showed synergistic effects when combined with 5-FU, a standard anticancer agent for PDAC. The present study is the first to report that laminarin exerts anticancer effect through ROS production in pancreatic cancer cells. Laminarin shows potential to serve as a new anticancer agent for treating PDAC. Full article
(This article belongs to the Special Issue Oxidative Stress Induced DNA Damage in Cancer Treatment)
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