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Cells
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Redox and Metabolic Profile of Cancer
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Redox and Metabolic Profile of Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 2587

Special Issue Editor

Dr. Bato Korac
*
E-Mail Website
Guest Editor
1. Institute for Biological Research "Sinisa Stankovic"—National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia
2. Faculty of Biology, University of Belgrade, Belgrade, Serbia
Interests: redox biology; metabolism; redox-metabolic (dys)functions in physiological and pathological conditions; cancer; hibernation; diabetes; aging; mitochondria
* Principal Scientist, Associate Professor

Special Issue Information

Dear Colleagues,

Life is a unity of opposites, and so is the case with aerobic organisms and their evolutionary expansion. With the presence of oxygen, organisms could maximally produce energy in metabolic processes, but reactive species (oxygen, nitrogen, sulfur, etc.) - which are formed as a metabolic ”by”-product, can be lethal - not only damaging major macromolecules but also potentially killing the cell. On the other hand, reactive species play a plethora of regulatory roles within cells and tissues. The evolutionarily conserved interplay between redox and cellular metabolism is strongly manifested in cancer growth.

Metabolic reprogramming of the tumor, discovered by Warburg about 100 years ago, is more relevant today than ever before. Nowadays, cancer is considered a metabolic disease, tightly coupled with redox homeostasis and characterized by an extraordinary capacity for redox-metabolic reprogramming. Metabolic reprogramming, either as a cause or a consequence of the tumorigenesis, is a hallmark characteristic of cancer from tumor initiation and progression to metastasis. Intriguingly, this metabolic switch is a feature not only of cancer cells but also of the surrounding cells in its microenvironment, which they shape together as they re-establish a new tissue homeostasis. To allow cancer growth, cancer cells have an increased need not only for energy but also for the biosynthesis of building blocks, and they generate a unique redox environment not simply to control oxidative stress but also to control the resources necessary for cancer survival.

This Special Issue, entitled “Redox and Metabolic Profile of Cancer”, invites original research and review articles to contribute to the elucidation of the molecular mechanisms of redox-metabolic reprogramming in cancer and the discovery of new therapeutic and research avenues.

Dr. Bato Korac
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at mdpi.longhoe.net 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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • cancer
  • metabolism
  • redox biology
  • redox-metabolic reprogramming
  • reactive species: oxygen, nitrogen, sulfur, etc
  • cancer microenvironment
  • cancer-tissue cooperation
  • mitochondria

Published Papers (2 papers)

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Research

22 pages, 3387 KiB  
Article
Polyamine Catabolism Revisited: Acetylpolyamine Oxidase Plays a Minor Role due to Low Expression
by Olga N. Ivanova, Anna V. Gavlina, Inna L. Karpenko, Martin A. Zenov, Svetlana S. Antseva, Natalia F. Zakirova, Vladimir T. Valuev-Elliston, George S. Krasnov, Irina T. Fedyakina, Pavel O. Vorobyev, Birke Bartosch, Sergey N. Kochetkov, Anastasiya V. Lipatova, Dmitry V. Yanvarev and Alexander V. Ivanov
Cells 2024, 13(13), 1134; https://doi.org/10.3390/cells13131134 - 1 Jul 2024
Viewed by 440
Abstract
Biogenic polyamines are ubiquitous compounds. Dysregulation of their metabolism is associated with the development of various pathologies, including cancer, hyperproliferative diseases, and infections. The canonical pathway of polyamine catabolism includes acetylation of spermine and spermidine and subsequent acetylpolyamine oxidase (PAOX)-mediated oxidation of acetylpolyamines [...] Read more.
Biogenic polyamines are ubiquitous compounds. Dysregulation of their metabolism is associated with the development of various pathologies, including cancer, hyperproliferative diseases, and infections. The canonical pathway of polyamine catabolism includes acetylation of spermine and spermidine and subsequent acetylpolyamine oxidase (PAOX)-mediated oxidation of acetylpolyamines (back-conversion) or their direct efflux from the cell. PAOX is considered to catalyze a non-rate-limiting catabolic step. Here, we show that PAOX transcription levels are extremely low in various tumor- and non-tumor cell lines and, in most cases, do not change in response to altered polyamine metabolism. Its enzymatic activity is undetectable in the majority of cell lines except for neuroblastoma and low passage glioblastoma cell lines. Treatment of A549 cells with N1,N11-diethylnorspermine leads to PAOX induction, but its contribution to polyamine catabolism remains moderate. We also describe two alternative enzyme isoforms and show that isoform 4 has diminished oxidase activity and isoform 2 is inactive. PAOX overexpression correlates with the resistance of cancer cells to genotoxic antitumor drugs, indicating that PAOX may be a useful therapeutic target. Finally, PAOX is dispensable for the replication of various viruses. These data suggest that a decrease in polyamine levels is achieved predominantly by the secretion of acetylated spermine and spermidine rather than by back-conversion. Full article
(This article belongs to the Special Issue Redox and Metabolic Profile of Cancer)
16 pages, 10805 KiB  
Article
Breast Cancer: Mitochondria-Centered Metabolic Alterations in Tumor and Associated Adipose Tissue
by Tamara Zakic, Andjelika Kalezic, Zorka Drvendzija, Mirjana Udicki, Tatjana Ivkovic Kapicl, Biljana Srdic Galic, Aleksandra Korac, Aleksandra Jankovic and Bato Korac
Cells 2024, 13(2), 155; https://doi.org/10.3390/cells13020155 - 15 Jan 2024
Cited by 2 | Viewed by 1351
Abstract
The close cooperation between breast cancer and cancer-associated adipose tissue (CAAT) shapes the malignant phenotype, but the role of mitochondrial metabolic reprogramming and obesity in breast cancer remains undecided, especially in premenopausal women. Here, we examined mitochondrial metabolic dynamics in paired biopsies of [...] Read more.
The close cooperation between breast cancer and cancer-associated adipose tissue (CAAT) shapes the malignant phenotype, but the role of mitochondrial metabolic reprogramming and obesity in breast cancer remains undecided, especially in premenopausal women. Here, we examined mitochondrial metabolic dynamics in paired biopsies of malignant versus benign breast tumor tissue and CAAT in normal-weight and overweight/obese premenopausal women. Lower protein level of pyruvate dehydrogenase and citrate synthase in malignant tumor tissue indicated decreased carbon flux from glucose into the Krebs cycle, whereas the trend was just the opposite in malignant CAAT. Simultaneously, stimulated lipolysis in CAAT of obese women was followed by upregulated β-oxidation, as well as fatty acid synthesis enzymes in both tumor tissue and CAAT of women with malignant tumors, corroborating their physical association. Further, protein level of electron transport chain complexes was generally increased in tumor tissue and CAAT from women with malignant tumors, respective to obesity. Preserved mitochondrial structure in malignant tumor tissue was also observed. However, mitochondrial DNA copy number and protein levels of PGC-1α were dependent on both malignancy and obesity in tumor tissue and CAAT. In conclusion, metabolic cooperation between breast cancer and CAAT in premenopausal women involves obesity-related, synchronized changes in mitochondrial metabolism. Full article
(This article belongs to the Special Issue Redox and Metabolic Profile of Cancer)
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