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Biology
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Metabolic Crosstalk in Tumours
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Metabolic Crosstalk in Tumours

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cancer Biology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 7861

Special Issue Editors

Dr. Lucie Brisson

E-Mail Website1 Website2 Website3
Guest Editor
UMR 1069 Nutrition, Growth and Cancer, Inserm, University of Tours, Tours, France
Interests: cancer metabolism; metastasis; autophagy; fatty acids
Dr. Jean-François Dumas

E-Mail Website1 Website2 Website3
Guest Editor
UMR 1069 Nutrition, Growth and Cancer, Inserm, University of Tours, Tours, France
Interests: cancer metabolism; mitochondria; cardiolipin; chemoresistance

Special Issue Information

Dear Colleagues,

Metabolic adaptation, a common feature of cancer and non-cancer cells of the tumour microenvironment, participates in tumour growth, metastatic dissemination and therapy resistance. A better characterization of metabolic pathways and interconnection in tumours can lead to the development of new anti-cancer targets in order to improve cancer therapy.

Major achievements have been done in the understanding of cancer progression considering tumour as a complex multi-cellular tissue surrounded by specific microenvironment. In tumours, cells are subjected to very strong selective pressures that lead to develop several strategies to adapt, especially through in depth interaction and exploitation of the tumour microenvironment. Only the most aggressive and metabolically adapted cells survive to this microenvironment, and to the stress that are generated by anticancer treatments.

Metabolic adaptation in tumours includes specific metabolic reprogramming, using metabolic substrate from surrounding microenvironment (lactate, fatty acids, glutamine…) and the activation of recycling pathways like macroautophagy and selective autophagy. In addition, complex interactions occur between these metabolic pathways and between cancer and non-cancer cells from the tumours. Although it is well recognized that metabolic adaptation promotes tumours progression and limits cancer treatments, the understanding of the metabolic interactions in tumours remains an important challenge in cancer research. A better characterization of tumour metabolic interactions within the tumour microenvironment is promising for the development of new anticancer strategies.

This special issue invites original and review papers covering the broad range of topics related to metabolic adaptations and metabolic interactions in tumours.

Dr. Lucie Brisson
Dr. Jean-François Dumas
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. Biology 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
  • tumour microenvironment
  • autophagy
  • cancer treatment
  • metastasis

Published Papers (3 papers)

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Research

Jump to: Review, Other

15 pages, 1802 KiB  
Article
The Long Non-Coding RNA SAMMSON Is a Regulator of Chemosensitivity and Metabolic Orientation in MCF-7 Doxorubicin-Resistant Breast Cancer Cells
by Charlotte Orre, Xavier Dieu, Jordan Guillon, Naïg Gueguen, Seyedeh Tayebeh Ahmadpour, Jean-François Dumas, Salim Khiati, Pascal Reynier, Guy Lenaers, Olivier Coqueret, Arnaud Chevrollier, Delphine Mirebeau-Prunier and Valérie Desquiret-Dumas
Biology 2021, 10(11), 1156; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10111156 - 09 Nov 2021
Cited by 12 | Viewed by 1789
Abstract
Despite improvements in therapeutic strategies for treating breast cancers, tumor relapse and chemoresistance remain major issues in patient outcomes. Indeed, cancer cells display a metabolic plasticity allowing a quick adaptation to the tumoral microenvironment and to cellular stresses induced by chemotherapy. Recently, long [...] Read more.
Despite improvements in therapeutic strategies for treating breast cancers, tumor relapse and chemoresistance remain major issues in patient outcomes. Indeed, cancer cells display a metabolic plasticity allowing a quick adaptation to the tumoral microenvironment and to cellular stresses induced by chemotherapy. Recently, long non-coding RNA molecules (lncRNAs) have emerged as important regulators of cellular metabolic orientation. In the present study, we addressed the role of the long non-coding RNA molecule (lncRNA) SAMMSON on the metabolic reprogramming and chemoresistance of MCF-7 breast cancer cells resistant to doxorubicin (MCF-7dox). Our results showed an overexpression of SAMMSON in MCF-7dox compared to doxorubicin-sensitive cells (MCF-7). Silencing of SAMMSON expression by siRNA in MCF-7dox cells resulted in a metabolic rewiring with improvement of oxidative metabolism, decreased mitochondrial ROS production, increased mitochondrial replication, transcription and translation and an attenuation of chemoresistance. These results highlight the role of SAMMSON in the metabolic adaptations leading to the development of chemoresistance in breast cancer cells. Thus, targeting SAMMSON expression levels represents a promising therapeutic route to circumvent doxorubicin resistance in breast cancers. Full article
(This article belongs to the Special Issue Metabolic Crosstalk in Tumours)
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Review

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18 pages, 1561 KiB  
Review
Oncometabolites—A Link between Cancer Cells and Tumor Microenvironment
by Maksymilian Baryła, Aleksandra Semeniuk-Wojtaś, Letycja Róg, Leszek Kraj, Maciej Małyszko and Rafał Stec
Biology 2022, 11(2), 270; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11020270 - 09 Feb 2022
Cited by 13 | Viewed by 2502
Abstract
The tumor microenvironment is the space between healthy tissues and cancer cells, created by the extracellular matrix, blood vessels, infiltrating cells such as immune cells, and cancer-associated fibroblasts. These components constantly interact and influence each other, enabling cancer cells to survive and develop [...] Read more.
The tumor microenvironment is the space between healthy tissues and cancer cells, created by the extracellular matrix, blood vessels, infiltrating cells such as immune cells, and cancer-associated fibroblasts. These components constantly interact and influence each other, enabling cancer cells to survive and develop in the host organism. Accumulated intermediate metabolites favoring dysregulation and compensatory responses in the cell, called oncometabolites, provide a method of communication between cells and might also play a role in cancer growth. Here, we describe the changes in metabolic pathways that lead to accumulation of intermediate metabolites: lactate, glutamate, fumarate, and succinate in the tumor and their impact on the tumor microenvironment. These oncometabolites are not only waste products, but also link all types of cells involved in tumor survival and progression. Oncometabolites play a particularly important role in neoangiogenesis and in the infiltration of immune cells in cancer. Oncometabolites are also associated with a disrupted DNA damage response and make the tumor microenvironment more favorable for cell migration. The knowledge summarized in this article will allow for a better understanding of associations between therapeutic targets and oncometabolites, as well as the direct effects of these particles on the formation of the tumor microenvironment. In the future, targeting oncometabolites could improve treatment standards or represent a novel method for fighting cancer. Full article
(This article belongs to the Special Issue Metabolic Crosstalk in Tumours)
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Other

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12 pages, 1212 KiB  
Opinion
Warburg Effect, Glutamine, Succinate, Alanine, When Oxygen Matters
by Frédéric Bouillaud, Noureddine Hammad and Laurent Schwartz
Biology 2021, 10(10), 1000; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10101000 - 04 Oct 2021
Cited by 6 | Viewed by 2727
Abstract
Cellular bioenergetics requires an intense ATP turnover that is increased further by hypermetabolic states caused by cancer growth or inflammation. Both are associated with metabolic alterations and, notably, enhancement of the Warburg effect (also known as aerobic glycolysis) of poor efficiency with regard [...] Read more.
Cellular bioenergetics requires an intense ATP turnover that is increased further by hypermetabolic states caused by cancer growth or inflammation. Both are associated with metabolic alterations and, notably, enhancement of the Warburg effect (also known as aerobic glycolysis) of poor efficiency with regard to glucose consumption when compared to mitochondrial respiration. Therefore, beside this efficiency issue, other properties of these two pathways should be considered to explain this paradox: (1) biosynthesis, for this only indirect effect should be considered, since lactate release competes with biosynthetic pathways in the use of glucose; (2) ATP production, although inefficient, glycolysis shows other advantages when compared to mitochondrial respiration and lactate release may therefore reflect that the glycolytic flux is higher than required to feed mitochondria with pyruvate and glycolytic NADH; (3) Oxygen supply becomes critical under hypermetabolic conditions, and the ATP/O2 ratio quantifies the efficiency of oxygen use to regenerate ATP, although aerobic metabolism remains intense the participation of anaerobic metabolisms (lactic fermentation or succinate generation) could greatly increase ATP/O2 ratio; (4) time and space constraints would explain that anaerobic metabolism is required while the general metabolism appears oxidative; and (5) active repression of respiration by glycolytic intermediates, which could ensure optimization of glucose and oxygen use. Full article
(This article belongs to the Special Issue Metabolic Crosstalk in Tumours)
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