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Antioxidants
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Free Radical Research in Cancer
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Free Radical Research in Cancer

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 (30 October 2019) | Viewed by 82743

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Ana Čipak Gašparović

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Guest Editor
Laboratory for Oxidative Stress, Institute Ruder Boskovic, Zagreb, Croatia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is a pleasure to invite you to contribute to this Special Issue of Antioxidants by submitting original research papers or review articles focusing on “Free Radical Research in Cancer”.

Cancer is a great challenge to efficient therapy due to biological diversity. Disturbed oxidative homeostasis in cancer cells certainly contributes to differential therapy response. One of the hallmarks of cancer cells is adaptation, which includes fine tuning of the cellular metabolic and signalling pathways, as well as transcription profiles. One of the factors causing rapid adaptation are changes in oxygen levels due to hypoxia/reoxygenation during growth changing antioxidative patterns as a consequence. Finally, these events sum up and create challenges for efficient cancer therapy.

The aim of this Special Issue is to present recent findings and to describe the state-of-the-art on the mechanisms by which free radicals contribute to cancer development and change response to therapy.

We look forward to receiving many contributions and stimulating a productive discussion on this exciting thematic of role of free radicals in cancer development, progression and treatment.

Best regards,

Dr. Ana Čipak Gašparović
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

  • free radicals
  • oxidative stress
  • ROS
  • RNS
  • cancer
  • cancer stem cells
  • cancer therapy
  • cell signalling
  • antioxidative transcription factors
  • drug delivery system

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Published Papers (12 papers)

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Editorial

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4 pages, 176 KiB  
Editorial
Free Radical Research in Cancer
by Ana Čipak Gašparović
Antioxidants 2020, 9(2), 157; https://doi.org/10.3390/antiox9020157 - 15 Feb 2020
Cited by 16 | Viewed by 3413
Abstract
It can be challenging to find efficient therapy for cancer due to its biological diversity [...] Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)

Research

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18 pages, 2456 KiB  
Article
Bardoxolone-Methyl (CDDO-Me) Suppresses Androgen Receptor and Its Splice-Variant AR-V7 and Enhances Efficacy of Enzalutamide in Prostate Cancer Cells
by Namrata Khurana, Partha K. Chandra, Hogyoung Kim, Asim B. Abdel-Mageed, Debasis Mondal and Suresh C. Sikka
Antioxidants 2020, 9(1), 68; https://doi.org/10.3390/antiox9010068 - 12 Jan 2020
Cited by 21 | Viewed by 5062
Abstract
Androgen receptor (AR) signaling is fundamental to prostate cancer (PC) progression, and hence, androgen deprivation therapy (ADT) remains a mainstay of treatment. However, augmented AR signaling via both full length AR (AR-FL) and constitutively active AR splice variants, especially AR-V7, is associated with [...] Read more.
Androgen receptor (AR) signaling is fundamental to prostate cancer (PC) progression, and hence, androgen deprivation therapy (ADT) remains a mainstay of treatment. However, augmented AR signaling via both full length AR (AR-FL) and constitutively active AR splice variants, especially AR-V7, is associated with the recurrence of castration resistant prostate cancer (CRPC). Oxidative stress also plays a crucial role in anti-androgen resistance and CRPC outgrowth. We examined whether a triterpenoid antioxidant drug, Bardoxolone-methyl, known as CDDO-Me or RTA 402, can decrease AR-FL and AR-V7 expression in PC cells. Nanomolar (nM) concentrations of CDDO-Me rapidly downregulated AR-FL in LNCaP and C4-2B cells, and both AR-FL and AR-V7 in CWR22Rv1 (22Rv1) cells. The AR-suppressive effect of CDDO-Me was evident at both the mRNA and protein levels. Mechanistically, acute exposure (2 h) to CDDO-Me increased and long-term exposure (24 h) decreased reactive oxygen species (ROS) levels in cells. This was concomitant with an increase in the anti-oxidant transcription factor, Nrf2. The anti-oxidant N-acetyl cysteine (NAC) could overcome this AR-suppressive effect of CDDO-Me. Co-exposure of PC cells to CDDO-Me enhanced the efficacy of a clinically approved anti-androgen, enzalutamide (ENZ), as evident by decreased cell-viability along with migration and colony forming ability of PC cells. Thus, CDDO-Me which is in several late-stage clinical trials, may be used as an adjunct to ADT in PC patients. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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18 pages, 3532 KiB  
Article
Chronic Oxidative Stress Promotes Molecular Changes Associated with Epithelial Mesenchymal Transition, NRF2, and Breast Cancer Stem Cell Phenotype
by Ana Čipak Gašparović, Lidija Milković, Nadia Dandachi, Stefanie Stanzer, Iskra Pezdirc, Josip Vrančić, Sanda Šitić, Christoph Suppan and Marija Balic
Antioxidants 2019, 8(12), 633; https://doi.org/10.3390/antiox8120633 - 11 Dec 2019
Cited by 30 | Viewed by 4820
Abstract
Oxidative stress plays a role in carcinogenesis, but it also contributes to the modulation of tumor cells and microenvironment caused by chemotherapeutics. One of the consequences of oxidative stress is lipid peroxidation, which can, through reactive aldehydes such as 4-hydroxy-2-nonenal (HNE), affect cell [...] Read more.
Oxidative stress plays a role in carcinogenesis, but it also contributes to the modulation of tumor cells and microenvironment caused by chemotherapeutics. One of the consequences of oxidative stress is lipid peroxidation, which can, through reactive aldehydes such as 4-hydroxy-2-nonenal (HNE), affect cell signaling pathways. On the other hand, cancer stem cells (CSC) are now recognized as a major factor of malignancy by causing metastasis, relapse, and therapy resistance. Here, we evaluated whether oxidative stress and HNE modulation of the microenvironment can influence CSC growth, modifications of the epithelial to mesenchymal transition (EMT) markers, the antioxidant system, and the frequency of breast cancer stem cells (BCSC). Our results showed that oxidative changes in the microenvironment of BCSC and particularly chronic oxidative stress caused changes in the proliferation and growth of breast cancer cells. In addition, changes associated with EMT, increase in glutathione (GSH) and Nuclear factor erythroid 2-related factor 2 (NRF2) were observed in breast cancer cells grown on HNE pretreated collagen and under chronic oxidative stress. Our results suggest that chronic oxidative stress can be a bidirectional modulator of BCSC fate. Low levels of HNE can increase differentiation markers in BCSC, while higher levels increased GSH and NRF2 as well as certain EMT markers, thereby increasing therapy resistance. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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14 pages, 2002 KiB  
Article
Combination of PDT and NOPDT with a Tailored BODIPY Derivative
by Loretta Lazzarato, Elena Gazzano, Marco Blangetti, Aurore Fraix, Federica Sodano, Giulia Maria Picone, Roberta Fruttero, Alberto Gasco, Chiara Riganti and Salvatore Sortino
Antioxidants 2019, 8(11), 531; https://doi.org/10.3390/antiox8110531 - 7 Nov 2019
Cited by 17 | Viewed by 3849
Abstract
The engineering of photosensitizers (PS) for photodynamic therapy (PDT) with nitric oxide (NO) photodonors (NOPD) is broadening the horizons for new and yet to be fully explored unconventional anticancer treatment modalities that are entirely controlled by light stimuli. In this work, we report [...] Read more.
The engineering of photosensitizers (PS) for photodynamic therapy (PDT) with nitric oxide (NO) photodonors (NOPD) is broadening the horizons for new and yet to be fully explored unconventional anticancer treatment modalities that are entirely controlled by light stimuli. In this work, we report a tailored boron-dipyrromethene (BODIPY) derivative that acts as a PS and a NOPD simultaneously upon single photon excitation with highly biocompatible green light. The photogeneration of the two key species for PDT and NOPDT, singlet oxygen (1O2) and NO, has been demonstrated by their direct detection, while the formation of NO is shown not to be dependent on the presence of oxygen. Biological studies carried out using A375 and SKMEL28 cancer cell lines, with the aid of suitable model compounds that are based on the same BODIPY light harvesting core, unambiguously reveal the combined action of 1O2 and NO in inducing amplified cancer cell mortality exclusively under irradiation with visible green light. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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14 pages, 10051 KiB  
Article
A Role for H2O2 and TRPM2 in the Induction of Cell Death: Studies in KGN Cells
by Carsten Theo Hack, Theresa Buck, Konstantin Bagnjuk, Katja Eubler, Lars Kunz, Doris Mayr and Artur Mayerhofer
Antioxidants 2019, 8(11), 518; https://doi.org/10.3390/antiox8110518 - 29 Oct 2019
Cited by 19 | Viewed by 4831
Abstract
Recent studies showed that KGN cells, derived from a human granulosa cell tumor (GCT), express NADPH oxidase 4 (NOX4), an important source of H2O2. Transient receptor potential melastatin 2 (TRPM2) channel is a Ca2+ permeable cation channel that [...] Read more.
Recent studies showed that KGN cells, derived from a human granulosa cell tumor (GCT), express NADPH oxidase 4 (NOX4), an important source of H2O2. Transient receptor potential melastatin 2 (TRPM2) channel is a Ca2+ permeable cation channel that can be activated by H2O2 and plays an important role in cellular functions. It is also able to promote susceptibility to cell death. We studied expression and functionality of TRPM2 in KGN cells and examined GCT tissue microarrays (TMAs) to explore in vivo relevance. We employed live cell, calcium and mitochondrial imaging, viability assays, fluorescence activated cell sorting (FACS) analysis, Western blotting and immunohistochemistry. We confirmed that KGN cells produce H2O2 and found that they express functional TRPM2. H2O2 increased intracellular Ca2+ levels and N-(p-Amylcinnamoyl)anthranilic acid (ACA), a TRPM2 inhibitor, blocked this action. H2O2 caused mitochondrial fragmentation and apoptotic cell death, which could be attenuated by a scavenger (Trolox). Immunohistochemistry showed parallel expression of NOX4 and TRPM2 in all 73 tumor samples examined. The results suggest that GCTs can be endowed with a system that may convey susceptibility to cell death. If so, induction of oxidative stress may be beneficial in GCT therapy. Our results also imply a therapeutic potential for TRPM2 as a drug target in GCTs. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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17 pages, 4746 KiB  
Article
Protein Carbonylation in Patients with Myelodysplastic Syndrome: An Opportunity for Deferasirox Therapy
by Alba Rodríguez-García, María Luz Morales, Vanesa Garrido-García, Irene García-Baquero, Alejandra Leivas, Gonzalo Carreño-Tarragona, Ricardo Sánchez, Alicia Arenas, Teresa Cedena, Rosa María Ayala, José M. Bautista, Joaquín Martínez-López and María Linares
Antioxidants 2019, 8(11), 508; https://doi.org/10.3390/antiox8110508 - 24 Oct 2019
Cited by 5 | Viewed by 4090
Abstract
Control of oxidative stress in the bone marrow (BM) is key for maintaining the interplay between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better [...] Read more.
Control of oxidative stress in the bone marrow (BM) is key for maintaining the interplay between self-renewal, proliferation, and differentiation of hematopoietic cells. Breakdown of this regulation can lead to diseases characterized by BM failure such as the myelodysplastic syndromes (MDS). To better understand the role of oxidative stress in MDS development, we compared protein carbonylation as an indicator of oxidative stress in the BM of patients with MDS and control subjects, and also patients with MDS under treatment with the iron chelator deferasirox (DFX). As expected, differences in the pattern of protein carbonylation were observed in BM samples between MDS patients and controls, with an increase in protein carbonylation in the former. Strikingly, patients under DFX treatment had lower levels of protein carbonylation in BM with respect to untreated patients. Proteomic analysis identified four proteins with high carbonylation levels in MDS BM cells. Finally, as oxidative stress-related signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment. Overall, our results suggest that the fine-tuning of oxidative stress levels in the BM of patients with MDS might control malignant progression. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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8 pages, 649 KiB  
Article
Cancer Chemotherapy and Chemiluminescence Detection of Reactive Oxygen Species in Human Semen
by Teppei Takeshima, Shinnosuke Kuroda and Yasushi Yumura
Antioxidants 2019, 8(10), 449; https://doi.org/10.3390/antiox8100449 - 1 Oct 2019
Cited by 6 | Viewed by 3188
Abstract
Advanced treatments have improved the prognosis of cancer survivors. Anticancer drugs generate large amounts of cellular reactive oxygen species (ROS), but their direct effects on sperm ROS production are unclear. We examined 64 semen samples of men who had received cancer chemotherapy, 467 [...] Read more.
Advanced treatments have improved the prognosis of cancer survivors. Anticancer drugs generate large amounts of cellular reactive oxygen species (ROS), but their direct effects on sperm ROS production are unclear. We examined 64 semen samples of men who had received cancer chemotherapy, 467 semen samples of men consulting for idiopathic infertility, and 402 semen samples of partners of female patients as a control group. ROS production was calculated as the integrated chemiluminescence between 0 and 200 seconds after the addition of luminol to unwashed semen. We found that their ROS-positive rate of semen samples in the chemotherapy group was significantly higher than that in the control group. We compared the sperm parameters (concentration and motility) and the ROS production levels between chemotherapy subgroups and one of the remaining subgroups with positive ROS, and we found that only sperm motility was significantly lower in the samples in the postchemotherapy subgroup than in the idiopathic infertility subgroup, and that both sperm parameters were significantly lower in those from postchemotherapy subgroup than in the control subgroup. The ROS production level per million spermatozoa in the postchemotherapy subgroup was significantly higher than that in the control subgroup. Additionally, we compared variables, such as age, sperm features, and the duration from the end of the treatment to the first consultation between ROS-positive and ROS-negative subgroups in samples from men in the postchemotherapy group, but we found no significant differences. Of the men in the postchemotherapy group, three underwent a long-term antioxidant therapy, and all of them had low ROS semen levels after that. In conclusion, the production of ROS in semen detected by chemiluminescence from men who undergo cancer chemotherapy is similar to that of men with idiopathic infertility, and long-term oral antioxidant therapy may reduce the amount of ROS in the semen. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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10 pages, 1693 KiB  
Article
Cancer Cell Sensitivity to Redox-Cycling Quinones is Influenced by NAD(P)H: Quinone Oxidoreductase 1 Polymorphism
by Christophe Glorieux and Pedro Buc Calderon
Antioxidants 2019, 8(9), 369; https://doi.org/10.3390/antiox8090369 - 2 Sep 2019
Cited by 21 | Viewed by 4948
Abstract
Background: Cancer cell sensitivity to drugs may be associated with disturbed antioxidant enzymes expression. We investigated mechanisms of resistance by using oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). Since nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase-1 (NQO1) is modified in tumors and [...] Read more.
Background: Cancer cell sensitivity to drugs may be associated with disturbed antioxidant enzymes expression. We investigated mechanisms of resistance by using oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). Since nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase-1 (NQO1) is modified in tumors and oxidative stress-resistant cells, we studied its role in cells exposed to β-lapachone, menadione, and doxorubicin. Methods: Normal mammary epithelial 250MK, MCF-7, and Resox cells were employed. NQO1 expression and enzyme activity were determined by quantitative polymerase chain reaction (RT-PCR), immunoblotting, and biochemical assays. Dicoumarol and gene silencing (siRNA) were used to modulate NQO1 expression and to assess its potential drug-detoxifying role. MTT (3-(4,5-dimethylthia-zolyl-2)-2,5-diphenyltetrazolium bromide) or clonogenic assays were used to investigate cytotoxicity. NQO1 variants, NQO1*1 (wt), and NQO1*2 (C609T), were obtained by transfecting NQO1-null MDA-MB-231 cell line. Results: Resox cells have higher NQO1 expression than MCF-7 cells. In 250MK cells its expression was low but enzyme activity was higher suggesting a variant NQO1 form in MCF-7 cells. MCF-7 and Resox cells are heterozygous NQO1*1 (wt)/NQO1*2 (C609T). Both NQO1 polymorphism and NQO1 overexpression are main determinants for cell resistance during oxidative stress. NQO1 overexpression increases cell sensitivity to β-lapachone whereas NQO1*2 polymorphism triggers quinone-based chemotherapies-sensitivity. Conclusions: NQO1 influences cancer cells redox metabolism and their sensitivity to drugs. We suggest that determining NQO1 polymorphism may be important when considering the use of quinone-based chemotherapeutic drugs. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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Review

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15 pages, 1429 KiB  
Review
Oxidative Stress and Cancer: Chemopreventive and Therapeutic Role of Triphala
by Sahdeo Prasad and Sanjay K. Srivastava
Antioxidants 2020, 9(1), 72; https://doi.org/10.3390/antiox9010072 - 13 Jan 2020
Cited by 61 | Viewed by 21048
Abstract
Oxidative stress, caused by the overproduction of free radicals, leads to the development of many chronic diseases including cancer. Free radicals are known to damage cellular biomolecules like lipids, proteins, and DNA that results in activation of multiple signaling pathways, growth factors, transcription [...] Read more.
Oxidative stress, caused by the overproduction of free radicals, leads to the development of many chronic diseases including cancer. Free radicals are known to damage cellular biomolecules like lipids, proteins, and DNA that results in activation of multiple signaling pathways, growth factors, transcription factors, kinases, inflammatory and cell cycle regulatory molecules. Antioxidants, which are classified as exogenous and endogenous, are responsible for the removal of free radicals and consequently the reduction in oxidative stress-mediated diseases. Diet and medicinal herbs are the major source of antioxidants. Triphala, which is a traditional Ayurvedic formulation that has been used for centuries, has been shown to have immense potential to boost antioxidant activity. It scavenges free radicals, restores antioxidant enzymes and non-enzyme levels, and decreases lipid peroxidation. In addition, Triphala is revered as a chemopreventive, chemotherapeutic, immunomodulatory, and radioprotective agent. Accumulated evidence has revealed that Triphala modulates multiple cell signaling pathways including, ERK, MAPK, NF-κB, Akt, c-Myc, VEGFR, mTOR, tubulin, p53, cyclin D1, anti-apoptotic and pro-apoptotic proteins. The present review focuses on the comprehensive appraisal of Triphala in oxidative stress and cancer. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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25 pages, 1131 KiB  
Review
Metabolic Remodelling: An Accomplice for New Therapeutic Strategies to Fight Lung Cancer
by Cindy Mendes and Jacinta Serpa
Antioxidants 2019, 8(12), 603; https://doi.org/10.3390/antiox8120603 - 29 Nov 2019
Cited by 14 | Viewed by 5111
Abstract
Metabolic remodelling is a hallmark of cancer, however little has been unravelled in its role in chemoresistance, which is a major hurdle to cancer control. Lung cancer is a leading cause of death by cancer, mainly due to the diagnosis at an advanced [...] Read more.
Metabolic remodelling is a hallmark of cancer, however little has been unravelled in its role in chemoresistance, which is a major hurdle to cancer control. Lung cancer is a leading cause of death by cancer, mainly due to the diagnosis at an advanced stage and to the development of resistance to therapy. Targeted therapeutic agents combined with comprehensive drugs are commonly used to treat lung cancer. However, resistance mechanisms are difficult to avoid. In this review, we will address some of those therapeutic regimens, resistance mechanisms that are eventually developed by lung cancer cells, metabolic alterations that have already been described in lung cancer and putative new therapeutic strategies, and the integration of conventional drugs and genetic and metabolic-targeted therapies. The oxidative stress is pivotal in this whole network. A better understanding of cancer cell metabolism and molecular adaptations underlying resistance mechanisms will provide clues to design new therapeutic strategies, including the combination of chemotherapeutic and targeted agents, considering metabolic intervenients. As cancer cells undergo a constant metabolic adaptive drift, therapeutic regimens must constantly adapt. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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20 pages, 1401 KiB  
Review
Modulation of Oxidative Stress by Ozone Therapy in the Prevention and Treatment of Chemotherapy-Induced Toxicity: Review and Prospects
by Bernardino Clavo, Francisco Rodríguez-Esparragón, Delvys Rodríguez-Abreu, Gregorio Martínez-Sánchez, Pedro Llontop, David Aguiar-Bujanda, Leandro Fernández-Pérez and Norberto Santana-Rodríguez
Antioxidants 2019, 8(12), 588; https://doi.org/10.3390/antiox8120588 - 26 Nov 2019
Cited by 75 | Viewed by 10494
Abstract
(1) Background: Cancer is one of the leading causes of mortality worldwide. Radiotherapy and chemotherapy attempt to kill tumor cells by different mechanisms mediated by an intracellular increase of free radicals. However, free radicals can also increase in healthy cells and lead to [...] Read more.
(1) Background: Cancer is one of the leading causes of mortality worldwide. Radiotherapy and chemotherapy attempt to kill tumor cells by different mechanisms mediated by an intracellular increase of free radicals. However, free radicals can also increase in healthy cells and lead to oxidative stress, resulting in further damage to healthy tissues. Approaches to prevent or treat many of these side effects are limited. Ozone therapy can induce a controlled oxidative stress able to stimulate an adaptive antioxidant response in healthy tissue. This review describes the studies using ozone therapy to prevent and/or treat chemotherapy-induced toxicity, and how its effect is linked to a modification of free radicals and antioxidants. (2) Methods: This review encompasses a total of 13 peer-reviewed original articles (most of them with assessment of oxidative stress parameters) and some related works. It is mainly focused on four drugs: Cisplatin, Methotrexate, Doxorubicin, and Bleomycin. (3) Results: In experimental models and the few existing clinical studies, modulation of free radicals and antioxidants by ozone therapy was associated with decreased chemotherapy-induced toxicity. (4) Conclusions: The potential role of ozone therapy in the management of chemotherapy-induced toxicity merits further research. Randomized controlled trials are ongoing. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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18 pages, 1640 KiB  
Review
Redox-Mediated Mechanism of Chemoresistance in Cancer Cells
by Eun-Kyung Kim, MinGyeong Jang, Min-Jeong Song, Dongwoo Kim, Yosup Kim and Ho Hee Jang
Antioxidants 2019, 8(10), 471; https://doi.org/10.3390/antiox8100471 - 10 Oct 2019
Cited by 115 | Viewed by 10024
Abstract
Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. [...] Read more.
Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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