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Novel Metabolism-Related Biomarkers in Cancer
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Novel Metabolism-Related Biomarkers in Cancer

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Bioorganic Chemistry".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 4395

Special Issue Editors

Dr. Maria de Fátima Monginho Baltazar

E-Mail Website
Guest Editor
1. School of Medicine, University of Minho, 4710-057 Braga, Portugal
2. ICVS/3B's PT Government Associate Laboratory, 4710-057 Braga, Portugal
Interests: cancer glycolytic metabolism; new metabolic biomarkers in cancer; cancer drug resistance; drug discovery in cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Julieta Alexandra Pereira Afonso

E-Mail Website
Guest Editor
1. School of Medicine, University of Minho, 4710-057 Braga, Portugal
2. ICVS/3B's PT Government Associate Laboratory, 4710-057 Braga, Portugal
Interests: bladder cancer; chemoresistance; immunotherapy resistance; cancer metabolism; Warburg effect; monocarboxylate transporters; CD147; tumor microenvironment; cancer-associated fibroblasts
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is a major global threat to public health, and validated, specific and sensitive cancer biomarkers are increasingly being used to accurately diagnose and manage cancer patients. However, patient treatment remains largely unsuccessful in the long term due to evolving metabolic alterations and intricate signaling within the challenging cancer microenvironment. Metabolic networks sustain fundamental cellular functions, from energy production to biosynthesis, to determine cellular fates. Distinct metabolic signatures are displayed by different cancer types, and increasing understanding of the hallmarks of metabolic reprogramming and plasticity in cancer cells is generating novel metabolism-related biomarkers that show promise in further advancing personalized medicine and improving patients’ outcomes. This Special Issue will highlight recent developments in cancer metabolism-related biomarkers’ discovery and validation, encompassing not only the historical Warburg fundamentals of the glycolytic phenotype, but also other metabolic patterns, such as amino acid, lipid and trace element metabolism, that will certainly contribute to deciphering cancer complexity and aid in directing future therapeutic interventions.

Dr. Maria de Fátima Monginho Baltazar
Dr. Julieta Alexandra Pereira Afonso
Guest Editors

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Keywords

  • cancer biomarkers
  • personalized medicine
  • metabolism
  • glucose
  • amino acid
  • glutamine
  • lipid
  • iron

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Published Papers (3 papers)

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Research

27 pages, 3015 KB  
Article
Effects of Asprosin and Role of TLR4 as a Biomarker in Endometrial Cancer
by Rebecca Karkia, Cristina Sisu, Sayeh Saravi, Ioannis Kyrou, Harpal S. Randeva, Jayanta Chatterjee and Emmanouil Karteris
Molecules 2025, 30(16), 3410; https://doi.org/10.3390/molecules30163410 - 18 Aug 2025
Viewed by 599
Abstract
(1) Background: Following the discovery of the adipokine/hormone asprosin, a substantial amount of research has provided evidence for its role in the regulation of glucose homeostasis, as well as appetite, and insulin sensitivity. Its levels are dysregulated in certain disease states, including breast [...] Read more.
(1) Background: Following the discovery of the adipokine/hormone asprosin, a substantial amount of research has provided evidence for its role in the regulation of glucose homeostasis, as well as appetite, and insulin sensitivity. Its levels are dysregulated in certain disease states, including breast cancer. To date, little is known about its role in endometrial cancer (EC). The present study investigated the effects of asprosin on the transcriptome of the Ishikawa and NOU-1 EC cell lines, and assessed the expression of asprosin’s candidate receptors (TLR4, PTPRD, and OR4M1) in health and disease. (2) Methods: tissue culture, RNA extraction, RNA sequencing, reverse transcription-quantitative PCR, gene enrichment and in silico analyses were used for this study. (3) Results: TLR4 and PTPRD were significantly downregulated in EC when compared to healthy controls. TLR4 appeared to have a prognostic role in terms of overall survival (OS) in EC patients (i.e., higher expression, better OS). RNA sequencing revealed that asprosin affected 289 differentially expressed genes (DEGs) in Ishikawa cells and 307 DEGs in NOU-1 cells. Pathway enrichment included apoptosis, glycolysis, hypoxia, and PI3K/AKT/ mTOR/NOTCH signalling for Ishikawa-treated cells. In NOU-1, enriched processes included inflammatory response, epithelial-mesenchymal transition, reactive oxygen species pathways, and interferon gamma responses. Other signalling pathways included mTORC1, DNA repair, and p53, amongst others. (4) Conclusions: These findings underscore the importance of understanding receptor dynamics and signalling pathways in the context of asprosin’s role in EC, and provide evidence for a potential role of TLR4 as a diagnostic biomarker. Full article
(This article belongs to the Special Issue Novel Metabolism-Related Biomarkers in Cancer)
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25 pages, 3010 KB  
Article
The Oncometabolite 2-Hydroxyglutarate Is Upregulated in Post-Prostatectomy PSA Recurrence of Prostate Cancer: A Metabolomic Analysis
by Dontrel W. Spencer Hairston, Shamira Sridharan-Weaver, Abheek Gandhi, Neelu Batra, Blythe P. Durbin-Johnson, Marc A. Dall’Era and Paramita M. Ghosh
Molecules 2025, 30(16), 3316; https://doi.org/10.3390/molecules30163316 - 8 Aug 2025
Viewed by 469
Abstract
First-line treatment for localized prostate cancer (PCa) includes radical prostatectomy (RP) for high-risk disease. However, in many cases, patients experience biochemical recurrence (BCR), heralded by rising prostate specific antigen (PSA) levels in the serum. Our goal was to identify metabolic pathways that are [...] Read more.
First-line treatment for localized prostate cancer (PCa) includes radical prostatectomy (RP) for high-risk disease. However, in many cases, patients experience biochemical recurrence (BCR), heralded by rising prostate specific antigen (PSA) levels in the serum. Our goal was to identify metabolic pathways that are disrupted in BCR to determine potential targets of therapy. We conducted metabolomic analysis in prostate tissue from the tumors of 74 patients who underwent prostatectomy as treatment for localized PCa and correlated levels of metabolites with clinical and non-clinical factors. Cholesterol and triglycerides were upregulated in Hispanic vs. non-Hispanic and in obese vs. non-obese individuals, respectively. Both lipids and non-lipids were altered with increasing Gleason grades and clinical stages. High post-RP PSA (>0.1 ng/mL) indicated recurrence (p = 0.0094) and correlated with alterations in 141 metabolites including 114 lipids and 26 non-lipid molecules. The largest increase with high post-RP PSA was in 2-hydroxyglutaric acid (2-HG), a product of the tricarboxylic acid (TCA) cycle, that had previously been established as an oncometabolite in other cancers. 2-HG was highly selective and specific for high post-RP PSA (AUC = 0.8526; p = 0.0002) while Kaplan–Meier curves indicated that among patients who recurred, high 2-HG in the tumor reduced time-to-recurrence from 84 months (for those with low 2-HG) to 38 months (for those with high 2-HG). The addition of D2HG, an enantiomer of 2-HG, increased the growth rate of LNCaP and C4 cells, and also increased Akt and ERK phosphorylation. 2-HG is upregulated in PCa tumors from patients who experience high post-RP PSA indicative of recurrence. Future studies may target this metabolite to prevent recurrent disease. Full article
(This article belongs to the Special Issue Novel Metabolism-Related Biomarkers in Cancer)
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32 pages, 6041 KB  
Article
Glucagon and Glucose Availability Influence Metabolic Heterogeneity and Malignancy in Pancreatic Neuroendocrine Tumour (pNET) Cells: Novel Routes for Therapeutic Targeting
by Bárbara Ferreira, Isabel Lemos, Cindy Mendes, Beatriz Chumbinho, Fernanda Silva, Daniela Pereira, Emanuel Vigia, Luís G. Gonçalves, António Figueiredo, Daniela Cavaco and Jacinta Serpa
Molecules 2025, 30(13), 2736; https://doi.org/10.3390/molecules30132736 - 25 Jun 2025
Viewed by 2960
Abstract
Cancer metabolism is a hallmark of cancer. However, the impact of systemic metabolism and diet on tumour evolution is less understood. This study delves into the role of glucagon, as a component of the pancreatic microenvironment, in regulating features of pancreatic neuroendocrine tumour [...] Read more.
Cancer metabolism is a hallmark of cancer. However, the impact of systemic metabolism and diet on tumour evolution is less understood. This study delves into the role of glucagon, as a component of the pancreatic microenvironment, in regulating features of pancreatic neuroendocrine tumour (pNET) cells and the metabolic remodelling occurring in the presence and absence of glucose. pNET cell lines (BON-1 and QGP-1) and the non-malignant pancreatic α-TC1 cell line were used as models. Results showed that pNET cells responded differently to glucose deprivation than α-TC1 cells. Specifically, pNET cells upregulated the GCGR in the absence of glucose, while α-TC1 cells did so in high-glucose conditions, allowing the glucagon-related pERK1/2 activation under these conditions in pNET cells. Glucagon enhanced cancerous features in pNET BON-1 cells under glucose-deprived and hyperglucagonemia-compatible concentrations. In the α-TC1 cell line, glucagon modulated cell features under high-glucose and physiological glucagon levels. NMR exometabolome analysis revealed differences in metabolic processes based on glucose availability and glucagon stimulation across cell lines, highlighting amino acid metabolism, glycolysis, and gluconeogenesis. The expression of metabolic genes was consistent with these findings. Interestingly, QGP-1 and α-TC1 cells produced glucose in no-glucose conditions, and glucagon upregulated glucose production in α-TC1 cells. This suggests that gluconeogenesis may be beneficial for some pNET subsets, pointing out novel metabolism-based strategies to manage pNETs, as well as a step forward in endocrinology and systemic metabolism. The association between GCGR expression and malignancy and a negative correlation between glucagon receptor (GCGR) and glucagon-like peptide-1 receptor (GLP-1R) expression was observed, indicating a biological role of glucagon in pNETs that deserves to be explored. Full article
(This article belongs to the Special Issue Novel Metabolism-Related Biomarkers in Cancer)
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