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Metabolites
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Reactive Oxygen Species and Energy Metabolic Alterations in Health and...
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Reactive Oxygen Species and Energy Metabolic Alterations in Health and Disease

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: 15 October 2025 | Viewed by 3050

Special Issue Editors

Dr. Paola Maycotte

E-Mail Website
Guest Editor
Centro de Investigación Biomédica de Oriente, Instituto Mexicano del Seguro Social, Puebla 74360, Mexico
Interests: cancer; metabolism; autophagy; reactive oxygen species; phytochemicals
Special Issues, Collections and Topics in MDPI journals
Dr. Álvaro Marín-Hernández

E-Mail Website1 Website2
Guest Editor
Departamento de Bioquímica, Instituto Nacional de Cardiología, Mexico City 14080, Mexico
Interests: mitochondria; intermediary metabolism; glycolysis; cancer; enzyme
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cellular alterations in energy metabolism and metabolic reprogramming are considered hallmarks of diverse diseases including cancer, neurodegenerative diseases and certainly, metabolic disorders like metabolic syndrome and diabetes. For example, an altered cellular metabolism has been recognized as one of the hallmarks of cancer since malignant cells are known to divert flux through their metabolic pathways (glycolysis, pentose phosphate pathway, Krebs cycle, etc.) to increase macromolecule and organelle biosynthesis to maintain active cellular proliferation. Recent research has associated some of these metabolic changes, particularly in mitochondria, to the production of reactive oxygen species (ROS), reactive oxygen by-products with a strong oxidation and signaling functions.

This Special Issue welcomes submissions of original research and reviews from diverse areas of cellular biology and biomedical research fields concerned with metabolic and ROS functions and alterations in human diseases, with the purpose of stimulating intriguing perspectives in the discipline.

Dr. Paola Maycotte
Dr. Álvaro Marín-Hernández
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. Metabolites 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 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
  • ROS
  • glycolysis
  • mitochondria
  • autophagy
  • antioxidant system
  • glutathione
  • oxidative phosphorylation

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Published Papers (2 papers)

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Research

17 pages, 1407 KiB  
Article
Metabolic Effects of the Cancer Metastasis Modulator MEMO1
by Marziyeh Ghanbarian, Natalia Dolgova, Frederick S. Vizeacoumar, Franco J. Vizeacoumar, Deborah Michel, Anas El-Aneed and Oleg Y. Dmitriev
Metabolites 2025, 15(4), 277; https://doi.org/10.3390/metabo15040277 - 17 Apr 2025
Viewed by 294
Abstract
Background/Objectives: Cancer cells often display altered energy metabolism. In particular, expression levels and activity of the tricarboxylic acid cycle (TCA cycle) enzymes may change in cancer, and dysregulation of the TCA cycle is a frequent hallmark of cancer cell metabolism. MEMO1, a modulator [...] Read more.
Background/Objectives: Cancer cells often display altered energy metabolism. In particular, expression levels and activity of the tricarboxylic acid cycle (TCA cycle) enzymes may change in cancer, and dysregulation of the TCA cycle is a frequent hallmark of cancer cell metabolism. MEMO1, a modulator of cancer metastasis, has been shown to bind iron and regulate iron homeostasis in the cells. MEMO1 knockout changed mitochondrial morphology and iron content in breast cancer cells. Our previous genome-wide analysis of MEMO1 genetic interactions across multiple cancer cell lines revealed that gene sets involved in mitochondrial respiration and the TCA cycle are enriched among the gain-of-function interaction partners of MEMO1. Based on these findings, we measured the TCA cycle metabolite levels in breast cancer cells with varying levels of MEMO1 expression. Methods: ShRNA knockdown assay was performed to test essentiality of key TCA cycle enzymes. TCA metabolites were quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in MDA-MB-231 (high MEMO1), M67-2 (MEMO1 knockdown), and M67-9 (MEMO1 knockout) cells under iron-depleted, basal iron, and iron-supplemented conditions. Results:ACO2 and OGDH knockdowns inhibit cell proliferation, indicating an essential role of the TCA cycle in MDA-MB-231 metabolism. α-Ketoglutarate and citrate levels exhibited an inverse relationship with MEMO1 expression, increasing significantly in MEMO1 knockout cells regardless of iron availability. In contrast, fumarate, malate, and glutamate levels were elevated in MEMO1 knockout cells specifically under low iron conditions, suggesting an iron-dependent effect. Conclusions: Overall, our results indicate that MEMO1 plays a role in regulating the TCA in cancer cells in an iron-dependent manner. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Energy Metabolic Alterations in Health and Disease)
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17 pages, 3381 KiB  
Article
Metabolic and Oxidative Stress Management Heterogeneity in a Panel of Breast Cancer Cell Lines
by Paola Maycotte, Fabiola Lilí Sarmiento-Salinas, Alin García-Miranda, Cesar Ivan Ovando-Ovando, Diana Xochiquetzal Robledo-Cadena, Luz Hernández-Esquivel, Ricardo Jasso-Chávez and Alvaro Marín-Hernández
Metabolites 2024, 14(8), 435; https://doi.org/10.3390/metabo14080435 - 6 Aug 2024
Cited by 1 | Viewed by 2241
Abstract
Metabolic alterations are recognized as one of the hallmarks of cancer. Among these, alterations in mitochondrial function have been associated with an enhanced production of Reactive Oxygen Species (ROS), which activate ROS-regulated cancer cell signaling pathways. Breast cancer is the main cancer-related cause [...] Read more.
Metabolic alterations are recognized as one of the hallmarks of cancer. Among these, alterations in mitochondrial function have been associated with an enhanced production of Reactive Oxygen Species (ROS), which activate ROS-regulated cancer cell signaling pathways. Breast cancer is the main cancer-related cause of death for women globally. It is a heterogeneous disease with subtypes characterized by specific molecular features and patient outcomes. With the purpose of identifying differences in energy metabolism and the oxidative stress management system in non-tumorigenic, estrogen receptor positive (ER+) and triple negative (TN) breast cancer cells, we evaluated ROS production, protein enzyme levels and activities and profiled energy metabolism. We found differences in energetic metabolism and ROS management systems between non-tumorigenic and cancer cells and between ER+ and TN breast cancer cells. Our results indicate a dependence on glycolysis despite different glycolytic ATP levels in all cancer cell lines tested. In addition, our data show that high levels of ROS in TN cells are a result of limited antioxidant capacity in the NADPH producing and GSH systems, mitochondrial dysfunction and non-mitochondrial ROS production, making them more sensitive to GSH synthesis inhibitors. Our data suggest that metabolic and antioxidant profiling of breast cancer will provide important targets for metabolic inhibitors or antioxidant treatments for breast cancer therapy. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Energy Metabolic Alterations in Health and Disease)
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