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Metabolites
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Cancer Associated Changes in Metabolism
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Cancer Associated Changes in Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Advances in Metabolomics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 12979

Special Issue Editors

Prof. Dr. Oliver Bathe

E-Mail Website
Guest Editor
Department of Oncology, University of Calgary, Calgary, AB T2N 4N2, Canada
Interests: biomarkers; metabolomics; surgical oncology; gastrointestinal oncology
Dr. Rattner Jodi

E-Mail Website
Guest Editor
International Agency for Research on Cancer (World Health Organization), Lyon, France
Interests: metabolomic features associated with diet and drugs

Special Issue Information

Dear Colleagues,

Cancer is associated with a broad array of metabolic changes in the tumor as well as in the host. Metabolic perturbations derived from the host may arise secondary to a number of factors. For example, metabolic and inflammatory mediators of tumor origin may elicit a response in the host, and that response can be modified by germ line variations. In addition, there are treatment-related perturbations. Finally, the metabolome may be influenced by the microbiome which, in turn, is affected by diet, environmental factors and disease. This Special Issue of Metabolites will explore the diverse metabolic features associated with cancer. We invite the submission of papers related to intratumoral metabolism, the host-derived metabolic response, the influence of the microbiome on metabolism as well as papers exploring the influence of cancer treatments on metabolism.

Prof. Dr. Oliver Bathe
Dr. Rattner Jodi
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.

Published Papers (5 papers)

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Research

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12 pages, 2683 KiB  
Article
Evaluation of Syrosingopine, an MCT Inhibitor, as Potential Modulator of Tumor Metabolism and Extracellular Acidification
by Chloe Buyse, Nicolas Joudiou, Aude Warscotte, Elena Richiardone, Lionel Mignion, Cyril Corbet and Bernard Gallez
Metabolites 2022, 12(6), 557; https://doi.org/10.3390/metabo12060557 - 17 Jun 2022
Cited by 15 | Viewed by 2320
Abstract
Extracellular acidification has been shown to be an important characteristic of invasive tumors, as it promotes invasion and migration but also resistance to treatments. Targeting transporters involved in the regulation of tumor pH constitutes a promising anti-tumor approach, as it would disrupt cellular [...] Read more.
Extracellular acidification has been shown to be an important characteristic of invasive tumors, as it promotes invasion and migration but also resistance to treatments. Targeting transporters involved in the regulation of tumor pH constitutes a promising anti-tumor approach, as it would disrupt cellular pH homeostasis and negatively impact tumor growth. In this study, we evaluated the impact of syrosingopine, an inhibitor of MCT1 and MCT4, as a modulator of tumor metabolism and extracellular acidification in human breast cancer (MDA-MB-231) and pharyngeal squamous cell carcinoma (FaDu) cell models. In both models in vitro, we observed that exposure to syrosingopine led to a decrease in the extracellular acidification rate, intracellular pH, glucose consumption, lactate secretion and tumor cell proliferation with an increase in the number of late apoptotic/necrotic cells. However, in vivo experiments using the MDA-MB-231 model treated with a daily injection of syrosingopine did not reveal any significant change in extracellular pH (pHe) (as measured using CEST-MRI) or primary tumor growth. Overall, our study suggests that targeting MCT could lead to profound changes in tumor cell metabolism and proliferation, and it warrants further research to identify candidates without off-target effects. Full article
(This article belongs to the Special Issue Cancer Associated Changes in Metabolism)
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13 pages, 1896 KiB  
Article
Increased Ammonium Toxicity in Response to Exogenous Glutamine in Metastatic Breast Cancer Cells
by Violet A. Kiesel, Madeline P. Sheeley, Shawn S. Donkin, Michael K. Wendt, Stephen D. Hursting and Dorothy Teegarden
Metabolites 2022, 12(5), 469; https://doi.org/10.3390/metabo12050469 - 23 May 2022
Viewed by 1962
Abstract
Several cancers, including breast cancers, show dependence on glutamine metabolism. The purpose of the present study was to determine the mechanistic basis and impact of differential glutamine metabolism in nonmetastatic and metastatic murine mammary cancer cells. Universally labeled 13C5-glutamine metabolic [...] Read more.
Several cancers, including breast cancers, show dependence on glutamine metabolism. The purpose of the present study was to determine the mechanistic basis and impact of differential glutamine metabolism in nonmetastatic and metastatic murine mammary cancer cells. Universally labeled 13C5-glutamine metabolic tracing, qRT-PCR, measures of reductive–oxidative balance, and exogenous ammonium chloride treatment were used to assess glutamine reprogramming. Results show that 4 mM media concentration of glutamine, compared with 2 mM, reduced viability only in metastatic cells, and that this decrease in viability was accompanied by increased incorporation of glutamine-derived carbon into the tricarboxylic acid (TCA) cycle. While increased glutamine metabolism in metastatic cells occurred in tandem with a decrease in the reduced/oxidized glutathione ratio, treatment with the antioxidant molecule N-acetylcysteine did not rescue cell viability. However, the viability of metastatic cells was more sensitive to ammonium chloride treatment compared with nonmetastatic cells, suggesting a role of metabolic reprogramming in averting nitrogen cytotoxicity in nonmetastatic cells. Overall, these results demonstrate the ability of nonmetastatic cancer cells to reprogram glutamine metabolism and that this ability may be lost in metastatic cells. Full article
(This article belongs to the Special Issue Cancer Associated Changes in Metabolism)
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18 pages, 16664 KiB  
Article
Lung Adenocarcinoma Transcriptomic Analysis Predicts Adenylate Kinase Signatures Contributing to Tumor Progression and Negative Patient Prognosis
by Jonathan A. Chacon-Barahona, Ivan A. Salladay-Perez and Nathan James Lanning
Metabolites 2021, 11(12), 859; https://doi.org/10.3390/metabo11120859 - 09 Dec 2021
Cited by 1 | Viewed by 2850
Abstract
The ability to detect and respond to hypoxia within a developing tumor appears to be a common feature amongst most cancers. This hypoxic response has many molecular drivers, but none as widely studied as Hypoxia-Inducible Factor 1 (HIF-1). Recent evidence suggests that HIF-1 [...] Read more.
The ability to detect and respond to hypoxia within a developing tumor appears to be a common feature amongst most cancers. This hypoxic response has many molecular drivers, but none as widely studied as Hypoxia-Inducible Factor 1 (HIF-1). Recent evidence suggests that HIF-1 biology within lung adenocarcinoma (LUAD) may be associated with expression levels of adenylate kinases (AKs). Using LUAD patient transcriptome data, we sought to characterize AK gene signatures related to lung cancer hallmarks, such as hypoxia and metabolic reprogramming, to identify conserved biological themes across LUAD tumor progression. Transcriptomic analysis revealed perturbation of HIF-1 targets to correlate with altered expression of most AKs, with AK4 having the strongest correlation. Enrichment analysis of LUAD tumor AK4 gene signatures predicts signatures involved in pyrimidine, and by extension, nucleotide metabolism across all LUAD tumor stages. To further discriminate potential drivers of LUAD tumor progression within AK4 gene signatures, partial least squares discriminant analysis was used at LUAD stage-stage interfaces, identifying candidate genes that may promote LUAD tumor growth or regression. Collectively, these results characterize regulatory gene networks associated with the expression of all nine human AKs that may contribute to underlying metabolic perturbations within LUAD and reveal potential mechanistic insight into the complementary role of AK4 in LUAD tumor development. Full article
(This article belongs to the Special Issue Cancer Associated Changes in Metabolism)
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Review

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30 pages, 2026 KiB  
Review
Reprogramming of Fatty Acid Metabolism in Gynaecological Cancers: Is There a Role for Oestradiol?
by Azilleo Kristo Mozihim, Ivy Chung, Nur Akmarina B. M. Said and Amira Hajirah Abd Jamil
Metabolites 2022, 12(4), 350; https://doi.org/10.3390/metabo12040350 - 14 Apr 2022
Cited by 4 | Viewed by 2872
Abstract
Gynaecological cancers are among the leading causes of cancer-related death among women worldwide. Cancer cells undergo metabolic reprogramming to sustain the production of energy and macromolecules required for cell growth, division and survival. Emerging evidence has provided significant insights into the integral role [...] Read more.
Gynaecological cancers are among the leading causes of cancer-related death among women worldwide. Cancer cells undergo metabolic reprogramming to sustain the production of energy and macromolecules required for cell growth, division and survival. Emerging evidence has provided significant insights into the integral role of fatty acids on tumourigenesis, but the metabolic role of high endogenous oestrogen levels and increased gynaecological cancer risks, notably in obesity, is less understood. This is becoming a renewed research interest, given the recently established association between obesity and incidence of many gynaecological cancers, including breast, ovarian, cervical and endometrial cancers. This review article, hence, comprehensively discusses how FA metabolism is altered in these gynaecological cancers, highlighting the emerging role of oestradiol on the actions of key regulatory enzymes of lipid metabolism, either directly through its classical ER pathways, or indirectly via the IGIFR pathway. Given the dramatic rise in obesity and parallel increase in the prevalence of gynaecological cancers among premenopausal women, further clarifications of the complex mechanisms underpinning gynaecological cancers are needed to inform future prevention efforts. Hence, in our review, we also highlight opportunities where metabolic dependencies can be exploited as viable therapeutic targets for these hormone-responsive cancers. Full article
(This article belongs to the Special Issue Cancer Associated Changes in Metabolism)
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Other

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18 pages, 3044 KiB  
Systematic Review
Changes in Metabolism as a Diagnostic Tool for Lung Cancer: Systematic Review
by Hanne Mariën, Elien Derveaux, Karolien Vanhove, Peter Adriaensens, Michiel Thomeer and Liesbet Mesotten
Metabolites 2022, 12(6), 545; https://doi.org/10.3390/metabo12060545 - 14 Jun 2022
Cited by 4 | Viewed by 1920
Abstract
Lung cancer is the leading cause of cancer-related mortality worldwide, with five-year survival rates varying from 3–62%. Screening aims at early detection, but half of the patients are diagnosed in advanced stages, limiting therapeutic possibilities. Positron emission tomography-computed tomography (PET-CT) is an essential [...] Read more.
Lung cancer is the leading cause of cancer-related mortality worldwide, with five-year survival rates varying from 3–62%. Screening aims at early detection, but half of the patients are diagnosed in advanced stages, limiting therapeutic possibilities. Positron emission tomography-computed tomography (PET-CT) is an essential technique in lung cancer detection and staging, with a sensitivity reaching 96%. However, since elevated 18F-fluorodeoxyglucose (18F-FDG) uptake is not cancer-specific, PET-CT often fails to discriminate between malignant and non-malignant PET-positive hypermetabolic lesions, with a specificity of only 23%. Furthermore, discrimination between lung cancer types is still impossible without invasive procedures. High mortality and morbidity, low survival rates, and difficulties in early detection, staging, and typing of lung cancer motivate the search for biomarkers to improve the diagnostic process and life expectancy. Metabolomics has emerged as a valuable technique for these pitfalls. Over 150 metabolites have been associated with lung cancer, and several are consistent in their findings of alterations in specific metabolite concentrations. However, there is still more variability than consistency due to the lack of standardized patient cohorts and measurement protocols. This review summarizes the identified metabolic biomarkers for early diagnosis, staging, and typing and reinforces the need for biomarkers to predict disease progression and survival and to support treatment follow-up. Full article
(This article belongs to the Special Issue Cancer Associated Changes in Metabolism)
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