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Control of the Antitumor Immune Response by Cancer Metabolism

The metabolic reprogramming of tumor cells and immune escape are two major hallmarks of cancer cells. The metabolic changes that occur during tumorigenesis, enabling survival and proliferation, are described for both solid and hematological malignancies. Concurrently, tumor cells have deployed mecha...

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Detalles Bibliográficos
Autores principales: Domblides, Charlotte, Lartigue, Lydia, Faustin, Benjamin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406288/
https://www.ncbi.nlm.nih.gov/pubmed/30708988
http://dx.doi.org/10.3390/cells8020104
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author Domblides, Charlotte
Lartigue, Lydia
Faustin, Benjamin
author_facet Domblides, Charlotte
Lartigue, Lydia
Faustin, Benjamin
author_sort Domblides, Charlotte
collection PubMed
description The metabolic reprogramming of tumor cells and immune escape are two major hallmarks of cancer cells. The metabolic changes that occur during tumorigenesis, enabling survival and proliferation, are described for both solid and hematological malignancies. Concurrently, tumor cells have deployed mechanisms to escape immune cell recognition and destruction. Additionally, therapeutic blocking of tumor-mediated immunosuppression has proven to have an unprecedented positive impact in clinical oncology. Increased evidence suggests that cancer metabolism not only plays a crucial role in cancer signaling for sustaining tumorigenesis and survival, but also has wider implications in the regulation of antitumor immune signaling through both the release of signaling molecules and the expression of immune membrane ligands. Here, we review these molecular events to highlight the contribution of cancer cell metabolic reprogramming on the shaping of the antitumor immune response.
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spelling pubmed-64062882019-03-19 Control of the Antitumor Immune Response by Cancer Metabolism Domblides, Charlotte Lartigue, Lydia Faustin, Benjamin Cells Review The metabolic reprogramming of tumor cells and immune escape are two major hallmarks of cancer cells. The metabolic changes that occur during tumorigenesis, enabling survival and proliferation, are described for both solid and hematological malignancies. Concurrently, tumor cells have deployed mechanisms to escape immune cell recognition and destruction. Additionally, therapeutic blocking of tumor-mediated immunosuppression has proven to have an unprecedented positive impact in clinical oncology. Increased evidence suggests that cancer metabolism not only plays a crucial role in cancer signaling for sustaining tumorigenesis and survival, but also has wider implications in the regulation of antitumor immune signaling through both the release of signaling molecules and the expression of immune membrane ligands. Here, we review these molecular events to highlight the contribution of cancer cell metabolic reprogramming on the shaping of the antitumor immune response. MDPI 2019-01-31 /pmc/articles/PMC6406288/ /pubmed/30708988 http://dx.doi.org/10.3390/cells8020104 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Domblides, Charlotte
Lartigue, Lydia
Faustin, Benjamin
Control of the Antitumor Immune Response by Cancer Metabolism
title Control of the Antitumor Immune Response by Cancer Metabolism
title_full Control of the Antitumor Immune Response by Cancer Metabolism
title_fullStr Control of the Antitumor Immune Response by Cancer Metabolism
title_full_unstemmed Control of the Antitumor Immune Response by Cancer Metabolism
title_short Control of the Antitumor Immune Response by Cancer Metabolism
title_sort control of the antitumor immune response by cancer metabolism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406288/
https://www.ncbi.nlm.nih.gov/pubmed/30708988
http://dx.doi.org/10.3390/cells8020104
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