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Antioxidants
Special Issues
Redox-Regulating Enzymes and Cancer
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Redox-Regulating Enzymes and 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 (31 August 2021) | Viewed by 16243

Special Issue Editors

Prof. Dr. Juan C. Mayo

E-Mail Website
Guest Editor
Departamento de Morfologia y Biologia Celular, Instituto Universitario Oncologico del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain
Interests: redox regulation; antioxidant enzymes; oxidative stress; prostate cancer; melatonin
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Rosa M. Sainz

E-Mail Website
Guest Editor
Universidad de Oviedo, Oviedo, Spain
Interests: redox regulation; antioxidant enzymes; cell signaling; prostate cancer; cell metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

While there is a wide consensus about the instrumental role of free radicals in the initiation of cancer, no such agreement exists in the case of the precise role that antioxidants play in the biology of cancer cells. Redox control has emerged as one of the most primitive and evolutionary conserved mechanisms in the regulation of protein function. Consequently, all factors involved in the control of redox homeostasis have attracted the scientific attention, as they play crucial roles in several pathologies, including cancer. Therefore, antioxidant enzymes, rate-limiting enzymes involved in the synthesis of antioxidants or free radical-generating proteins have received attention regarding cancer. Antioxidants have been reported as preventive agents but have also been linked to poor prognosis in certain tumors. Similarly, antioxidant enzymes have also been shown to display dual roles in cancer. Thus, given the controversy about the real impact of redox control in tumor progression, the topic requires a modern view as well as a reconsideration that would provide biologists and clinicians with a better understanding of its importance in cancer. This Special Issue will aim to collect current scientific data as well as in-depth reviews focused on any aspects relating redox regulation and cancer.

Prof. Dr. Juan C. Mayo
Prof. Dr. Rosa M. Sainz
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.

Published Papers (4 papers)

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Research

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15 pages, 2047 KiB  
Article
Androgen-Dependent Prostate Cancer Cells Reprogram Their Metabolic Signature upon GLUT1 Upregulation by Manganese Superoxide Dismutase
by Isabel Quiros-Gonzalez, Pedro Gonzalez-Menendez, Juan C. Mayo, David Hevia, Francisco Artime-Naveda, Sheila Fernandez-Vega, Mario Fernandez-Fernandez, Pablo Rodriguez-Gonzalez, José I. Garcia-Alonso and Rosa M. Sainz
Antioxidants 2022, 11(2), 313; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020313 - 04 Feb 2022
Cited by 5 | Viewed by 2176
Abstract
Prostate cancer is the second leading cause of cancer in men across the globe. The prostate gland accounts for some unique glycolytic metabolic characteristics, which causes the metabolic features of prostate tumor initiation and progression to remain poorly characterized. The mitochondrial superoxide dismutase [...] Read more.
Prostate cancer is the second leading cause of cancer in men across the globe. The prostate gland accounts for some unique glycolytic metabolic characteristics, which causes the metabolic features of prostate tumor initiation and progression to remain poorly characterized. The mitochondrial superoxide dismutase (SOD2) is one of the major redox metabolism regulators. This study points out SOD2 as one major regulator for both redox and glycolytic metabolism in prostate cancer. SOD2 overexpression increases glucose transporter GLUT-1 and glucose uptake. This is not an insulin-mediated effect and seems to be sex-dependent, being present in male mice only. This event concurs with a series of substantial metabolic rearrangements at cytoplasmic and mitochondrial level. A concomitant decrease in glycolytic and pentose phosphate activity, and an increase in electron transfer in the mitochondrial electronic chain, were observed. The Krebs Cycle is altered to produce amino-acid intermediates by decreasing succinate dehydrogenase. This in turn generates a 13-fold increase in the oncometabolite succinate. The protein energy sensor AMPK is decreased at basal and phosphorylated levels in response to glucose deprivation. Finally, preliminary results in prostate cancer patients indicate that glandular areas presenting high levels of SOD2 show a very strong correlation with GLUT-1 protein levels (R2 = 0.287 p-value < 0.0001), indicating that in patients there may exist an analogous phenomenon to those observed in cell culture and mice. Full article
(This article belongs to the Special Issue Redox-Regulating Enzymes and Cancer)
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16 pages, 5674 KiB  
Article
LW1497, an Inhibitor of Malate Dehydrogenase, Suppresses TGF-β1-Induced Epithelial-Mesenchymal Transition in Lung Cancer Cells by Downregulating Slug
by Hyun Ji Kim, Mi Kyung Park, Hyun Jung Byun, Minkyoung Kim, Boram Kim, Lu Yu, Tuan Minh Nguyen, Thi Ha Nguyen, Phuong Anh Do, Eun Ji Kim, Ji Hyun Kim, Enkhmend Enkhtaivan, Kyung Sung Kim, Ji Yun Jang, Gyeoung Jin Kang, Ho Lee, Misun Won, Kyeong Lee, Jungsook Cho and Chang Hoon Lee
Antioxidants 2021, 10(11), 1674; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111674 - 24 Oct 2021
Cited by 4 | Viewed by 2536
Abstract
LW1497 suppresses the expression of the hypoxia-inducing factor (HIF)-1α inhibiting malate dehydrogenase. Although hypoxia and HIF-1α are known to be important in cancer, LW1497 has not been therapeutically applied to cancer yet. Thus, we investigated the effect of LW1497 on the epithelial-mesenchymal transition [...] Read more.
LW1497 suppresses the expression of the hypoxia-inducing factor (HIF)-1α inhibiting malate dehydrogenase. Although hypoxia and HIF-1α are known to be important in cancer, LW1497 has not been therapeutically applied to cancer yet. Thus, we investigated the effect of LW1497 on the epithelial-mesenchymal transition (EMT) of lung cancer cells. A549 and H1299 lung cancer cells were induced to undergo via TGF-β1 treatment, resulting in the downregulation of E-cadherin and upregulation of N-cadherin and Vimentin concurrently with increases in the migration and invasion capacities of the cells. These effects of TGF-β1 were suppressed upon co-treatment of the cells with LW1497. An RNA-seq analysis revealed that LW1497 induced differential expression of genes related to hypoxia, RNA splicing, angiogenesis, cell migration, and metastasis in the A549 lung cancer cell lines. We confirmed the differential expression of Slug, an EMT-related transcription factor. Results from Western blotting and RT-PCR confirmed that LW1497 inhibited the expression of EMT markers and Slug. After orthotopically transplanting A549 cancer cells into mice, LW1497 was administered to examine whether the lung cancer progression was inhibited. We observed that LW1497 reduced the area of cancer. In addition, the results from immunohistochemical analyses showed that LW1497 downregulated EMT markers and Slug. In conclusion, LW1497 suppresses cancer progression through the inhibition of EMT by downregulating Slug. Full article
(This article belongs to the Special Issue Redox-Regulating Enzymes and Cancer)
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16 pages, 1576 KiB  
Article
Glutamine Modulates Expression and Function of Glucose 6-Phosphate Dehydrogenase via NRF2 in Colon Cancer Cells
by Ibrahim H. Polat, Míriam Tarrado-Castellarnau, Adrian Benito, Claudia Hernandez-Carro, Josep Centelles, Silvia Marin and Marta Cascante
Antioxidants 2021, 10(9), 1349; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091349 - 25 Aug 2021
Cited by 14 | Viewed by 4053
Abstract
Nucleotide pools need to be constantly replenished in cancer cells to support cell proliferation. The synthesis of nucleotides requires glutamine and 5-phosphoribosyl-1-pyrophosphate produced from ribose-5-phosphate via the oxidative branch of the pentose phosphate pathway (ox-PPP). Both PPP and glutamine also play a key [...] Read more.
Nucleotide pools need to be constantly replenished in cancer cells to support cell proliferation. The synthesis of nucleotides requires glutamine and 5-phosphoribosyl-1-pyrophosphate produced from ribose-5-phosphate via the oxidative branch of the pentose phosphate pathway (ox-PPP). Both PPP and glutamine also play a key role in maintaining the redox status of cancer cells. Enhanced glutamine metabolism and increased glucose 6-phosphate dehydrogenase (G6PD) expression have been related to a malignant phenotype in tumors. However, the association between G6PD overexpression and glutamine consumption in cancer cell proliferation is still incompletely understood. In this study, we demonstrated that both inhibition of G6PD and glutamine deprivation decrease the proliferation of colon cancer cells and induce cell cycle arrest and apoptosis. Moreover, we unveiled that glutamine deprivation induce an increase of G6PD expression that is mediated through the activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2). This crosstalk between G6PD and glutamine points out the potential of combined therapies targeting oxidative PPP enzymes and glutamine catabolism to combat colon cancer. Full article
(This article belongs to the Special Issue Redox-Regulating Enzymes and Cancer)
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Review

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16 pages, 2540 KiB  
Review
A Systematic Review of Serum γ-Glutamyltransferase as a Prognostic Biomarker in Patients with Genitourinary Cancer
by Kosuke Takemura, Philip G. Board and Fumitaka Koga
Antioxidants 2021, 10(4), 549; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10040549 - 01 Apr 2021
Cited by 23 | Viewed by 6708
Abstract
γ-Glutamyltransferase (GGT), a membrane-bound enzyme, contributes to the metabolism of glutathione (GSH), which plays a critical physiological role in protecting cells against oxidative stress. GGT has been proposed as a biomarker of carcinogenesis and tumor progression given that GGT activity is important during [...] Read more.
γ-Glutamyltransferase (GGT), a membrane-bound enzyme, contributes to the metabolism of glutathione (GSH), which plays a critical physiological role in protecting cells against oxidative stress. GGT has been proposed as a biomarker of carcinogenesis and tumor progression given that GGT activity is important during both the promotion and invasion phases in cancer cells. Moreover, GGT expression is reportedly related to drug-resistance possibly because a wide range of drugs are conjugated with GSH, the availability of which is influenced by GGT activity. While serum GGT activity is commonly used as a quick, inexpensive, yet reliable means of assessing liver function, recent epidemiological studies have shown that it may also be an indicator of an increased risk of prostate cancer development. Moreover, elevated serum GGT is reportedly an adverse prognostic predictor in patients with urologic neoplasms, including renal cell carcinoma, prostate cancer, and urothelial carcinoma, although the background mechanisms have still not been well-characterized. The present review article summarizes the possible role of GGT in cancer cells and focuses on evidence evaluation through a systematic review of the latest literature on the prognostic role of serum GGT in patients with genitourinary cancer. Full article
(This article belongs to the Special Issue Redox-Regulating Enzymes and Cancer)
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