Metabolites and Cancer Signaling

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 5566

Special Issue Editors

1. Department of Pathological, Cytological and Thanatological Anatomy, ESS|P.PORTO, Porto, Portugal
2. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
3. ICVS/3Bs-PT Government Associate Laboratory, 4805-017 Guimarães, Portugal
Interests: solid tumors; tumor cell metabolism; oncobiology; lactate transporters
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Guest Editor
1. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
2. ICVS/3Bs-PT Government Associate Laboratory, 4805-017 Guimarães, Portugal
Interests: brain tumors; cell signaling; glioblastoma; WNT pathway; HOX genes

Special Issue Information

Dear Colleagues,

Metabolites are not only end products of biosynthetic pathways but also important players in intercellular communication in the tumor microenvironment. Furthermore, increasing evidence has pointed to the fact that metabolites are signaling molecules controlling several features of cancer aggressiveness.

This Special Issue aims to highlight the relationship between metabolites and cancer signaling and how different metabolites in the tumor microenvironment promote tumor aggressiveness, namely their relation with the regulation of the malignant transformation, cell proliferation, epithelial-to-mesenchymal transition, differentiation blockade, cancer stemness, and therapy resistance. In this Special Issue, we welcome high-quality original research and review articles focusing on (but not limited to) the following subtopics:

  1. Oncometabolites as signaling molecules;
  2. Metabolic symbiosis in the tumor microenvironment mediated by Metabolites;
  3. The role of metabolites in drug resistance;
  4. Oncometabolites and immunosurveillance;
  5. Microbiota-derived metabolites in cancer;
  6. Signaling pathways as regulators of cancer cells metabolism.

Dr. Sara Granja
Dr. Céline S. Gonçalves
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 (2 papers)

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Review

13 pages, 614 KiB  
Review
Fatty Acid Metabolites and the Tumor Microenvironment as Potent Regulators of Cancer Stem Cell Signaling
by Toshiyuki Murai and Satoru Matsuda
Metabolites 2023, 13(6), 709; https://doi.org/10.3390/metabo13060709 - 31 May 2023
Cited by 3 | Viewed by 1750
Abstract
Individual cancer cells are not equal but are organized into a cellular hierarchy in which only a rare few leukemia cells can self-renew in a manner reminiscent of the characteristic stem cell properties. The PI3K/AKT pathway functions in a variety of cancers and [...] Read more.
Individual cancer cells are not equal but are organized into a cellular hierarchy in which only a rare few leukemia cells can self-renew in a manner reminiscent of the characteristic stem cell properties. The PI3K/AKT pathway functions in a variety of cancers and plays a critical role in the survival and proliferation of healthy cells under physiologic conditions. In addition, cancer stem cells might exhibit a variety of metabolic reprogramming phenotypes that cannot be completely attributed to the intrinsic heterogeneity of cancer. Given the heterogeneity of cancer stem cells, new strategies with single-cell resolution will become a powerful tool to eradicate the aggressive cell population harboring cancer stem cell phenotypes. Here, this article will provide an overview of the most important signaling pathways of cancer stem cells regarding their relevance to the tumor microenvironment and fatty acid metabolism, suggesting valuable strategies among cancer immunotherapies to inhibit the recurrence of tumors. Full article
(This article belongs to the Special Issue Metabolites and Cancer Signaling)
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13 pages, 4345 KiB  
Review
Targeting Ferroptosis in Colorectal Cancer
by Xiaojie Liang, Zhihuan You, Xinhao Chen and Jun Li
Metabolites 2022, 12(8), 745; https://doi.org/10.3390/metabo12080745 - 12 Aug 2022
Cited by 7 | Viewed by 3199
Abstract
Ferroptosis is a unique way of regulating cell death (RCD), which is quite different from other programmed cell deaths such as autophagy. It presents iron overload, accumulation of reactive oxygen species (ROS), and lipid peroxidation. A ferroptotic cell usually has an intact cell [...] Read more.
Ferroptosis is a unique way of regulating cell death (RCD), which is quite different from other programmed cell deaths such as autophagy. It presents iron overload, accumulation of reactive oxygen species (ROS), and lipid peroxidation. A ferroptotic cell usually has an intact cell structure as well as shrinking mitochondria with decreased or vanishing cristae, concentrated membrane density, and ruptured outer membrane. Recently, increasing investigations have discovered that tumor cells have a much greater iron demand than the normal ones, making them more sensitive to ferroptosis. In other words, ferroptosis may inhibit the progress of the tumor, which can be used in the therapy of tumor patients, especially for those with chemotherapy resistance. Therefore, ferroptosis has become one hot spot in the field of tumor research in recent years. Colorectal cancer (CRC) is one common type of gastrointestinal malignancy. The incidence of CRC appears to have an upward trend year by year since the enhancement of living standards. Although surgery and chemoradiotherapy have largely improved the prognosis of patients with CRC, some patients still appear to have severe adverse reactions and drug resistance. Moreover, much research has verified that ferroptosis has a necessary association with the occurrence and progression of gastrointestinal tumors. In this review, we provide a comprehensive evaluation of the main mechanisms of iron metabolism, lipid metabolism, and amino acid metabolism involved in the occurrence of ferroptosis, as well as the research progress of ferroptosis in CRC. Full article
(This article belongs to the Special Issue Metabolites and Cancer Signaling)
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