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Metabolites
Special Issues
Insights into Tumor Cell Metabolism and Epigenetics
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Insights into Tumor Cell Metabolism and Epigenetics

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1499

Special Issue Editors

Dr. Sara Granja

E-Mail Website
Guest Editor
Department of Pathological, Cytological and Thanatological Anatomy, ESS-P. PORTO, Porto, Portugal
Interests: cancer metabolism; immunometabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Vera Miranda-Gonçalves

E-Mail Website
Guest Editor
Cancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP), RISE@CI-IPOP (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto), Porto Comprehensive Cancer Centre (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072 Porto, Portugal
Interests: epigenetics; cancer metabolism
Dr. Filipa Vieira

E-Mail Website
Guest Editor
Department of Pathological, Cytological and Thanatological Anatomy, ESS-P. PORTO, Porto, Portugal
Interests: epigenetics; oncobiology

Special Issue Information

Dear Colleagues,

Tumor cell metabolism is a complex and dynamic field in cancer research. Research in tumor cell metabolism is rapidly evolving, and ongoing studies aim to unravel the complexity of metabolic reprogramming in different cancer types. The intersection of cancer metabolism and epigenetics alterations represents a fascinating area of research that sheds light on how metabolic alterations influence the epigenetic landscape in cancer cells and vice versa.

The intricate interplay between cancer metabolism and epigenetics highlights the complexity of cancer biology. This Special Issue aims to unravel these connections, potentially identifying new therapeutic avenues and biomarkers for diagnosis, prognosis, and treatment response in cancer patients. In this Special Issue, we welcome high-quality original research and review articles focusing on (but not limited to) the following topics: crosstalk between metabolism and epigenetics; metabolic reprogramming and epigenetics; therapeutic strategies; and biomarkers for diagnosis, prognosis, and treatment response. 

Dr. Sara Granja
Dr. Vera Miranda-Gonçalves
Dr. Filipa Vieira
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

  • Warburg effect
  • epigenetic alterations
  • metabolic reprogramming
  • epigenome
  • transcriptional regula-tion
  • fatty acid metabolism

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Published Papers (2 papers)

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28 pages, 4577 KiB  
Article
Cell-Free DNA (cfDNA) Regulates Metabolic Remodeling in the ES-2 Ovarian Carcinoma Cell Line, Influencing Cell Proliferation, Quiescence, and Chemoresistance in a Cell-of-Origin-Specific Manner
by Isabel Lemos, Catarina Freitas-Dias, Ana Hipólito, José Ramalho, Fabrizio Carteni, Luís G. Gonçalves, Stefano Mazzoleni and Jacinta Serpa
Metabolites 2025, 15(4), 244; https://doi.org/10.3390/metabo15040244 - 2 Apr 2025
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Abstract
Background: The cell-free DNA (cfDNA) is an extracellular fragmented DNA found in body fluids in physiological and pathophysiological contexts. In cancer, cfDNA has been pointed out as a marker for disease diagnosis, staging, and prognosis; however, little is known about its biological role. [...] Read more.
Background: The cell-free DNA (cfDNA) is an extracellular fragmented DNA found in body fluids in physiological and pathophysiological contexts. In cancer, cfDNA has been pointed out as a marker for disease diagnosis, staging, and prognosis; however, little is known about its biological role. Methods: The role of cfDNA released by ES-2 ovarian cancer cells was investigated, along with the impact of glucose bioavailability and culture duration in the cfDNA-induced phenotype. The effect of cfDNA on ES-2 cell proliferation was evaluated by proliferation curves, and cell migration was assessed through wound healing. We explored the impact of different cfDNA variants on ES-2 cells’ metabolic profile using nuclear magnetic resonance (NMR) spectroscopy and cisplatin resistance through flow cytometry. Moreover, we assessed the protein levels of DNA-sensitive Toll-like receptor 9 (TLR9) by immunofluorescence and its colocalization with lysosome-associated membrane protein 1 (LAMP1). Results: This study demonstrated that despite inducing similar effects, different variants of cfDNA promote different effects on cells derived from the ES-2 cell line. We observed instant reactions of adopting the metabolic profile that brings back the cell functioning of more favorable culture conditions supporting proliferation and resembling the cell of origin of the cfDNA variant, as observed in unselected ES-2 cells. However, as a long-term selective factor, certain cfDNA variants induced quiescence that favors the chemoresistance of a subset of cancer cells. Conclusions: Therefore, different tumoral microenvironments may generate cfDNA variants that will impact cancer cells differently, orchestrating the disease fate. Full article
(This article belongs to the Special Issue Insights into Tumor Cell Metabolism and Epigenetics)
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23 pages, 8711 KiB  
Article
Cell-Free DNA (cfDNA) Regulates Metabolic Remodeling, Sustaining Proliferation, Quiescence, and Migration in MDA-MB-231, a Triple-Negative Breast Carcinoma (TNBC) Cell Line
by Isabel Lemos, Catarina Freitas-Dias, Ana Hipólito, José Ramalho, Fabrizio Carteni, Luís G. Gonçalves, Stefano Mazzoleni and Jacinta Serpa
Metabolites 2025, 15(4), 227; https://doi.org/10.3390/metabo15040227 - 27 Mar 2025
Viewed by 488
Abstract
Background: The clinical relevance of circulating cell-free DNA (cfDNA) in oncology has gained significant attention, with its potential as a biomarker for cancer diagnosis and monitoring. However, its precise role in cancer biology and progression remains unclear. cfDNA in cancer patients’ blood has [...] Read more.
Background: The clinical relevance of circulating cell-free DNA (cfDNA) in oncology has gained significant attention, with its potential as a biomarker for cancer diagnosis and monitoring. However, its precise role in cancer biology and progression remains unclear. cfDNA in cancer patients’ blood has been shown to activate signaling pathways, such as those mediated by toll-like receptors (TLRs), suggesting its involvement in cancer cell adaptation to the tumor microenvironment. Methods: This impact of cfDNA released from MDA-MB-231, a triple-negative breast cancer (TNBC) cell line was assessed, focusing on glucose availability and culture duration. The impact of cfDNA on the proliferation of MDA-MB-231 cells was investigated using proliferation curves, while cellular migration was evaluated through wound healing assays. The metabolic alterations induced by distinct cfDNA variants in MDA-MB-231 cells were investigated through nuclear magnetic resonance (NMR) spectroscopy, and their effect on cisplatin resistance was evaluated using flow cytometry. Furthermore, the expression levels of DNA-sensitive Toll-like receptor 9 (TLR9) were quantified via immunofluorescence, alongside its colocalization with lysosome-associated membrane protein 1 (LAMP1). Results: This study indicates that cfDNA facilitates metabolic adaptation, particularly under metabolic stress, by modulating glucose and glutamine consumption, key pathways in tumor cell metabolism. Exposure to cfDNA induced distinct metabolic shifts, favoring energy production through oxidative phosphorylation. The anti-cancer activity of cfDNA isolated from conditioned media of cells cultured under stressful conditions is influenced by the culture duration, emphasizing the importance of adaptation and se-lection in releasing cfDNA that can drive pro-tumoral processes. Additionally, cfDNA exposure influenced cell proliferation, quiescence, and migration, processes linked to metastasis and treatment resistance. These findings underscore cfDNA as a key mediator of metabolic reprogramming and adaptive responses in cancer cells, contributing to tumor progression and therapy resistance. Furthermore, the activation of TLR9 signaling suggests a mechanistic basis for cfDNA-induced phenotypic changes. Conclusions: Overall, cfDNA serves as a crucial signaling molecule in the tumor microenvironment, orchestrating adaptive processes that enhance cancer cell survival and progression. Full article
(This article belongs to the Special Issue Insights into Tumor Cell Metabolism and Epigenetics)
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