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Cancers
Special Issues
Targeting Metabolic Vulnerabilities in Cancer
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Targeting Metabolic Vulnerabilities in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (30 July 2024) | Viewed by 13611

Special Issue Editors

Dr. Francesca Ricci

E-Mail Website
Guest Editor
Istituto di Ricerche Farmacologiche Mario Negri-IRCCS, Mialn, Italy
Interests: preclinical models; DNA repair; cancer metabolism
Dr. Laura Brunelli

E-Mail Website
Guest Editor
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
Interests: protein; metabolite biomarker

Special Issue Information

Dear Colleagues,

Metabolism has recently emerged as a new potential therapeutic target in oncology. Altered metabolic pathways are crucial for tumor development and growth, including increased glucose uptake, glycolytic rates, OXPHOS activities and lipid production. In the last years, these perturbations have been exploited in order to increase the therapeutic response. Different pharmacological strategies targeting metabolic networks, as well as the use of particular diet regimens combined with treatment, have been developed and have shown promising efficacy in both preclinical and clinical studies.

This Special Issue aims to increase the knowledge of the different therapeutic approaches that target cancer metabolic perturbations in order to increase the response to therapy and avoid the development of resistance. The submission of manuscripts approaching innovative therapeutic strategies targeting cancer metabolism, as well as the presentation of new preclinical models useful for this kind of research, is encouraged. Translational research studies and systematic and perspective reviews are also welcome.

Dr. Francesca Ricci
Dr. Laura Brunelli
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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
  • targeting metabolic vulnerabilities
  • diet regimens
  • resistance to therapy
  • animal models
  • preclinical models

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Published Papers (4 papers)

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Research

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21 pages, 3176 KiB  
Article
Restricting Colorectal Cancer Cell Metabolism with Metformin: An Integrated Transcriptomics Study
by Ayla Orang, Shashikanth Marri, Ross A. McKinnon, Janni Petersen and Michael Z. Michael
Cancers 2024, 16(11), 2055; https://doi.org/10.3390/cancers16112055 - 29 May 2024
Cited by 2 | Viewed by 3268
Abstract
Background: Metformin is a first-line therapy for type 2 diabetes as it disrupts cellular metabolism. Despite the association between metformin and lower cancer incidence, the anti-tumour activity of the drug in colorectal cancer (CRC) is incompletely understood. This study identifies underlying molecular mechanisms [...] Read more.
Background: Metformin is a first-line therapy for type 2 diabetes as it disrupts cellular metabolism. Despite the association between metformin and lower cancer incidence, the anti-tumour activity of the drug in colorectal cancer (CRC) is incompletely understood. This study identifies underlying molecular mechanisms by which metformin slows colorectal cancer cell proliferation by investigating metformin-associated microRNA (miRNA) and target gene pairs implicated in signalling pathways. Methods: The present study analysed changes in miRNAs and the coding transcriptome in CRC cells treated with a sublethal dose of metformin, followed by the contextual validation of potential miRNA–target gene pairs. Results: Analyses of small RNA and transcriptome sequencing data revealed 104 miRNAs and 1221 mRNAs to be differentially expressed in CRC cells treated with metformin for 72 h. Interaction networks between differentially expressed miRNAs and putative target mRNAs were identified. Differentially expressed genes were mainly implicated in metabolism and signalling processes, such as the PI3K-Akt and MAPK/ERK pathways. Further validation of potential miRNA–target mRNA pairs revealed that metformin induced miR-2110 and miR-132-3p to target PIK3R3 and, consequently, regulate CRC cell proliferation, cell cycle progression and the PI3K-Akt signalling pathway. Metformin also induced miR-222-3p and miR-589-3p, which directly target STMN1 to inhibit CRC cell proliferation and cell cycle progression. Conclusions: This study identified novel changes in the coding transcriptome and small non-coding RNAs associated with metformin treatment of CRC cells. Integration of these datasets highlighted underlying mechanisms by which metformin impedes cell proliferation in CRC. Importantly, it identified the post-transcriptional regulation of specific genes that impact both metabolism and cell proliferation. Full article
(This article belongs to the Special Issue Targeting Metabolic Vulnerabilities in Cancer)
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Review

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15 pages, 1823 KiB  
Review
Hitting the Sweet Spot: How Glucose Metabolism Is Orchestrated in Space and Time by Phosphofructokinase-1
by Melissa Campos and Lauren V. Albrecht
Cancers 2024, 16(1), 16; https://doi.org/10.3390/cancers16010016 - 19 Dec 2023
Cited by 7 | Viewed by 3357
Abstract
Glycolysis is the central metabolic pathway across all kingdoms of life. Intensive research efforts have been devoted to understanding the tightly orchestrated processes of converting glucose into energy in health and disease. Our review highlights the advances in knowledge of how metabolic and [...] Read more.
Glycolysis is the central metabolic pathway across all kingdoms of life. Intensive research efforts have been devoted to understanding the tightly orchestrated processes of converting glucose into energy in health and disease. Our review highlights the advances in knowledge of how metabolic and gene networks are integrated through the precise spatiotemporal compartmentalization of rate-limiting enzymes. We provide an overview of technically innovative approaches that have been applied to study phosphofructokinase-1 (PFK1), which represents the fate-determining step of oxidative glucose metabolism. Specifically, we discuss fast-acting chemical biology and optogenetic tools that have delineated new links between metabolite fluxes and transcriptional reprogramming, which operate together to enact tissue-specific processes. Finally, we discuss how recent paradigm-shifting insights into the fundamental basis of glycolytic regulatory control have shed light on the mechanisms of tumorigenesis and could provide insight into new therapeutic vulnerabilities in cancer. Full article
(This article belongs to the Special Issue Targeting Metabolic Vulnerabilities in Cancer)
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24 pages, 2208 KiB  
Review
Lipid Metabolic Reprogramming in Embryonal Neoplasms with MYCN Amplification
by Jyotirmayee Talapatra and Mamatha M. Reddy
Cancers 2023, 15(7), 2144; https://doi.org/10.3390/cancers15072144 - 4 Apr 2023
Cited by 4 | Viewed by 2761
Abstract
Tumor cells reprogram their metabolism, including glucose, glutamine, nucleotide, lipid, and amino acids to meet their enhanced energy demands, redox balance, and requirement of biosynthetic substrates for uncontrolled cell proliferation. Altered lipid metabolism in cancer provides lipids for rapid membrane biogenesis, generates the [...] Read more.
Tumor cells reprogram their metabolism, including glucose, glutamine, nucleotide, lipid, and amino acids to meet their enhanced energy demands, redox balance, and requirement of biosynthetic substrates for uncontrolled cell proliferation. Altered lipid metabolism in cancer provides lipids for rapid membrane biogenesis, generates the energy required for unrestricted cell proliferation, and some of the lipids act as signaling pathway mediators. In this review, we focus on the role of lipid metabolism in embryonal neoplasms with MYCN dysregulation. We specifically review lipid metabolic reactions in neuroblastoma, retinoblastoma, medulloblastoma, Wilms tumor, and rhabdomyosarcoma and the possibility of targeting lipid metabolism. Additionally, the regulation of lipid metabolism by the MYCN oncogene is discussed. Full article
(This article belongs to the Special Issue Targeting Metabolic Vulnerabilities in Cancer)
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21 pages, 2083 KiB  
Review
Host Microbiomes Influence the Effects of Diet on Inflammation and Cancer
by Ramsha Mahmood, Athalia Voisin, Hana Olof, Reihane Khorasaniha, Samuel A. Lawal and Heather K. Armstrong
Cancers 2023, 15(2), 521; https://doi.org/10.3390/cancers15020521 - 14 Jan 2023
Cited by 1 | Viewed by 3229
Abstract
Cancer is the second leading cause of death globally, and there is a growing appreciation for the complex involvement of diet, microbiomes, and inflammatory processes culminating in tumorigenesis. Although research has significantly improved our understanding of the various factors involved in different cancers, [...] Read more.
Cancer is the second leading cause of death globally, and there is a growing appreciation for the complex involvement of diet, microbiomes, and inflammatory processes culminating in tumorigenesis. Although research has significantly improved our understanding of the various factors involved in different cancers, the underlying mechanisms through which these factors influence tumor cells and their microenvironment remain to be completely understood. In particular, interactions between the different microbiomes, specific dietary factors, and host cells mediate both local and systemic immune responses, thereby influencing inflammation and tumorigenesis. Developing an improved understanding of how different microbiomes, beyond just the colonic microbiome, can interact with dietary factors to influence inflammatory processes and tumorigenesis will support our ability to better understand the potential for microbe-altering and dietary interventions for these patients in future. Full article
(This article belongs to the Special Issue Targeting Metabolic Vulnerabilities in Cancer)
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