Special Issue "Molecular Links between Cancer and Metabolic Diseases: New Perspectives and Therapeutic Strategies for Cancer Prevention and Treatment by Targeting Nutritional Patterns and Metabolic Alterations"

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

Deadline for manuscript submissions: 31 March 2022.

Special Issue Editors

Prof. Dr. Hamid Morjani
E-Mail Website
Guest Editor
Faculty of Pharmacy, University of Reims, BioSpecT EA7506, F-54000 Nancy, France
Interests: cellular and tumour microenvironement factors mediating cell proliferation and survival
Prof. Dr. Mohamed Zaiou
E-Mail Website
Guest Editor
School of Pharmacy & The Institute of Jean-Lamour, The University of Lorraine, UMR 7198 CNRS, CEDEX, 54505 Vandoeuvre les Nancy, France
Interests: gene expression; metabolic diseases; biomarkers; epigenetics; precision medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer and metabolic disease are among the leading causes of death worldwide. Beside genomic instability, accumulating evidence from epidemiological and prospective has linked nutrition and metabolic disorders such as diabetes, obesity, nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome, to increased risk for the development of several types of cancer. For instance, the incidence of gastrointestinal, and reproductive tract cancers is significantly higher in patients with metabolic abnormalities as compared to the general population. Moreover, evidence suggests that diabetes may affect cancer biology via hyperglycemia and hyperinsulinemia.

The mechanisms linking metabolic dysregulation and some cancers incidence and progression are incompletely understood. Acceleration of the global nutrition transition, the food system transformation and the increase in metabolic abnormalities could be among contributors to increased relative risk of cancer. Furthermore, metabolic diseases are characterized by low grade of persistent inflammation, a critical factor that is also involved in cancer initiation and progression.

Researchers now view new strategies for metabolomics research as promising fields that are likely to shed light on cancer etiology and diagnostic biomarker profiles, particularly for different cancers including colorectum, liver, pancreas, and breast cancer. Bioactive dietary components with anticancer properties are of particular interest as they may influence gene expression through epigenetic mechanisms and therefore some of them may be used in conjunction with other cancer prevention and chemotherapeutic therapies. Finally, the convergence of cancer cellular mechanisms and alterations in signaling pathways that control metabolism and proliferation on one hand and overall metabolic alterations suggest that new prevention and therapeutic strategies should target key effectors responsible for both cancer and metabolic diseases.

This Special Issue of “Cancers” will focus on the biological links between metabolic diseases (diabetes, obesity, NAFLD, metabolic syndrome, …) and some cancers, and that from genetic and epigenetic drivers and nutritional and metabolic point of view. Original articles, reviews, meta-analyses/systematic review, and case reports that address up-to-date and relevant findings with respect to the above area are welcome. Finally, on a personal side, we look forward with excitement to what the future holds for these complex and challenging potentially connected multigenic diseases (metabolic diseases and some cancers).

Prof. Dr. Hamid Morjani
Prof. Dr. Mohamed Zaiou
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 papers will be 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. 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 2400 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

  • metabolic diseases
  • colorectal cancer
  • oral cancer
  • obesity
  • metabolic pathways
  • nutrients
  • dietary intervention, molecular profiles, diagnosis and prognosis
  • LAFLD
  • hepatocellular carcinoma (HCC)

Published Papers

This special issue is now open for submission, see below for planned papers.

Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Neuraminidase-1: a sialidase involved in the development of metabolic diseases and cancers
Authors: Kévin Toussaint; Aline Appert-Collin; Hamid Morjani; Hervé Sartelet; Béatrice Romier-Crouzet; Pascal Maurice; Laurent Duca; Sébastien Blaise; Amar Bennasroune
Affiliation: CNRS UMR 7369, Matrice Extracellulaire et Dynamique Cellulaire, MEDyC, Reims, France. Hamid Morjani: Unité BioSpecT, EA7506, Reims, France.
Abstract: Sialidases or neuraminidases (NEU) are glycosidases which cleaves terminal sialic acid residues from glycoproteins, glycolipids and oligosaccharides. Four types of mammalian sialidases, encoded by different genes have been described with distinct substrate specificity and subcellular localization: NEU-1, NEU-2, NEU-3, and NEU-4. Among them, NEU-1 identified in lysosomes and at the plasma membrane regulates many membrane receptors by desialylation resulting in either activation or inhibition of these receptors. At the plasma membrane, NEU-1 also associates with the elastin-binding protein and the carboxypeptidase protective protein/cathepsin A to form the elastin receptor complex. Activation of NEU-1 is required for elastogenesis and signal transduction through this receptor and is responsible for the biological effects mediated by the elastin-derived peptides (EDP) on atherosclerosis, thrombosis, insulin resistance and non-alcoholic steatohepatitis. Furthermore, NEU-1 is known to regulate breast cancer cells’ proliferation and invasion: indeed, EDP enhance human breast cancer cell invasiveness by increasing the activity of matrix metalloproteinases 2 and 14. Additional studies also highlighted an inhibition of tumor neovascularization growth and metastasis under oseltamivir phosphate treatment blocking NEU-1 in a mouse model of human triple-negative breast cancer. In melanoma, EDP promote cell invasion. EDP and NEU-1 are also involved in other cancer types notably in the development of hepatocellular carcinoma and ovarian cancer. All these data demonstrate that NEU-1 plays a significant role not only in the development of several cancers but also in metabolic disorders which make NEU-1 a pharmacological target of high potential in these physiopathological contexts.

Title: The good, the bad and the new about uric acid
Authors: Marcella Camici, Mercedes Garcia-Gil, Simone Allegrini, Maria Grazia Tozzi
Affiliation: Department of Biology, University of Pisa
Abstract: Uric acid is the final product of the purine catabolism. Its concentration in blood is sex-, age- and diet-dependent and close to its maximal solubility, indicating that it plays some important role. Indeed it was demonstrated that, at physiological concentrations, it is a powerful antioxidant and is a scavenger of singlet oxygen and radicals. In addition, uric acid is a good effector of several proteins involved in metabolic regulation and signaling. Recently, the relationship between uric acid and cancer has been extensively investigated. In this review we present the more recent results on the positive and negative effects played by uric acid in different cancer types and some new findings and hypotheses about the implication of this metabolite in the pathogenesis of several diseases including cancer.

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