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Metabolites
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Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment
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Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment

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

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 17004

Special Issue Editor

Dr. Raffaele Ivan Cincione

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, Faculty of Medicine and Surgery, University of Foggia, Foggia, 71122 Puglia, Italy
Interests: ketogenic; diet; low-carb diet; mitochondrial dysfunction; adjuvant metabolic therapy; diabetes; obesity; cancer nutritional support

Special Issue Information

Dear Colleagues,

A possible emerging approach to cancer treatment involves the targeting of aberrant tumor metabolism. The metabolic changes that occur throughout the progression of cancer provide distinct characteristics that can be used for therapeutic purposes, specifically targeting the metabolic demands of neoplastic cells for essential nutrients. As no tumor can grow without anabolic substrates or energy, their simultaneous inhibition could ultimately reduce the viability of most, if not all, neoplastic cells. Normal eukaryotic animal cells are metabolically flexible and can generate energy using substrate-level phosphorylation or mitochondrial oxidative phosphorylation, based on the availability of oxygen. Otherwise, cancer cells are largely dependent on the substrate-level phosphorylation of glucose and glutamine through the glycolysis and glutaminolysis pathways, regardless of the presence of oxygen. Exploiting these specific energy and metabolic characteristics of neoplastic cells, it is possible to implement a nutritional and pharmacological intervention aimed at reducing the main substrate-level phosphorylation energy substrates, i.e. glucose and glutamine, in order to obtain the production of non-fermentable substrates by neoplastic cells (e.g., ketone bodies) due to cancer’s mitochondrial dysfunction. This Special Issue will explore the therapeutic possibilities that emerge from cancer-disrupted metabolism and metabolic communication, acting through nutritional, metabolic, and pharmaceutical approaches, to precisely target abnormal tumor metabolism.

Dr. Raffaele Ivan Cincione
Guest Editor

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 metabolism
  • glycolysis
  • glutaminolysis
  • ketone bodies
  • mitochondrial dysfunction

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Published Papers (3 papers)

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Research

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18 pages, 2962 KiB  
Article
Lipidomics by Nuclear Magnetic Resonance Spectroscopy and Liquid Chromatography–High-Resolution Mass Spectrometry in Osteosarcoma: A Pilot Study
by João Guilherme de Moraes Pontes, Milka Jadranin, Márcia Regina Assalin, Melissa Quintero Escobar, Danijela Stanisic, Tássia Brena Barroso Carneiro Costa, André van Helvoort Lengert, Érica Boldrini, Sandra Regina Morini da Silva, Daniel Onofre Vidal, Leticia Huan Bacellar Liu, Mariana Maschietto and Ljubica Tasic
Metabolites 2024, 14(8), 416; https://doi.org/10.3390/metabo14080416 - 28 Jul 2024
Viewed by 1259
Abstract
Cancer is a complex disease that can also affect the younger population; however, it is responsible for a relatively high mortality rate of children and youth, especially in low- and middle-income countries (LMICs). Besides that, lipidomic studies in this age range are scarce. [...] Read more.
Cancer is a complex disease that can also affect the younger population; however, it is responsible for a relatively high mortality rate of children and youth, especially in low- and middle-income countries (LMICs). Besides that, lipidomic studies in this age range are scarce. Therefore, we analyzed blood serum samples from young patients (12 to 35 years) with bone sarcoma (osteosarcoma) and compared their lipidomics to the ones from the control group of samples, named healthy control (HC group), using NMR and LC-MS techniques. Furthermore, differences in the lipidomic profiles between OS patients with and without metastasis indicate higher glycerophosphocholine (GPC) and glycerophospholipid (GPL) levels in osteosarcoma and increased cholesterol, choline, polyunsaturated fatty acids (PUFAs), and glycerols during the metastasis. These differences, detected in the peripheral blood, could be used as biomarkers for liquid biopsy. Full article
(This article belongs to the Special Issue Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment)
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Review

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19 pages, 1774 KiB  
Review
Bile Acids in Pancreatic Carcinogenesis
by Bharti Sharma, Kate Twelker, Cecilia Nguyen, Scott Ellis, Navin D. Bhatia, Zachary Kuschner, Andrew Agriantonis, George Agriantonis, Monique Arnold, Jasmine Dave, Juan Mestre, Zahra Shafaee, Shalini Arora, Hima Ghanta and Jennifer Whittington
Metabolites 2024, 14(7), 348; https://doi.org/10.3390/metabo14070348 - 21 Jun 2024
Viewed by 1411
Abstract
Pancreatic cancer (PC) is a dangerous digestive tract tumor that is becoming increasingly common and fatal. The most common form of PC is pancreatic ductal adenocarcinoma (PDAC). Bile acids (BAs) are closely linked to the growth and progression of PC. They can change [...] Read more.
Pancreatic cancer (PC) is a dangerous digestive tract tumor that is becoming increasingly common and fatal. The most common form of PC is pancreatic ductal adenocarcinoma (PDAC). Bile acids (BAs) are closely linked to the growth and progression of PC. They can change the intestinal flora, increasing intestinal permeability and allowing gut microbes to enter the bloodstream, leading to chronic inflammation. High dietary lipids can increase BA secretion into the duodenum and fecal BA levels. BAs can cause genetic mutations, mitochondrial dysfunction, abnormal activation of intracellular trypsin, cytoskeletal damage, activation of NF-κB, acute pancreatitis, cell injury, and cell necrosis. They can act on different types of pancreatic cells and receptors, altering Ca2+ and iron levels, and related signals. Elevated levels of Ca2+ and iron are associated with cell necrosis and ferroptosis. Bile reflux into the pancreatic ducts can speed up the kinetics of epithelial cells, promoting the development of pancreatic intraductal papillary carcinoma. BAs can cause the enormous secretion of Glucagon-like peptide-1 (GLP-1), leading to the proliferation of pancreatic β-cells. Using Glucagon-like peptide-1 receptor agonist (GLP-1RA) increases the risk of pancreatitis and PC. Therefore, our objective was to explore various studies and thoroughly examine the role of BAs in PC. Full article
(This article belongs to the Special Issue Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment)
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Other

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24 pages, 2543 KiB  
Hypothesis
Mitochondrial–Stem Cell Connection: Providing Additional Explanations for Understanding Cancer
by Pierrick Martinez, Ilyes Baghli, Géraud Gourjon and Thomas N. Seyfried
Metabolites 2024, 14(4), 229; https://doi.org/10.3390/metabo14040229 - 17 Apr 2024
Viewed by 13936
Abstract
The cancer paradigm is generally based on the somatic mutation model, asserting that cancer is a disease of genetic origin. The mitochondrial–stem cell connection (MSCC) proposes that tumorigenesis may result from an alteration of the mitochondria, specifically a chronic oxidative phosphorylation (OxPhos) insufficiency [...] Read more.
The cancer paradigm is generally based on the somatic mutation model, asserting that cancer is a disease of genetic origin. The mitochondrial–stem cell connection (MSCC) proposes that tumorigenesis may result from an alteration of the mitochondria, specifically a chronic oxidative phosphorylation (OxPhos) insufficiency in stem cells, which forms cancer stem cells (CSCs) and leads to malignancy. Reviewed evidence suggests that the MSCC could provide a comprehensive understanding of all the different stages of cancer. The metabolism of cancer cells is altered (OxPhos insufficiency) and must be compensated by using the glycolysis and the glutaminolysis pathways, which are essential to their growth. The altered mitochondria regulate the tumor microenvironment, which is also necessary for cancer evolution. Therefore, the MSCC could help improve our understanding of tumorigenesis, metastases, the efficiency of standard treatments, and relapses. Full article
(This article belongs to the Special Issue Metabolic Cancer Therapy: Targeting Tumor Metabolism for Innovative Adjuvant Treatment)
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