The therapeutic implications of immunosuppressive tumor aerobic glycolysis.


Journal

Cellular & molecular immunology
ISSN: 2042-0226
Titre abrégé: Cell Mol Immunol
Pays: China
ID NLM: 101242872

Informations de publication

Date de publication:
01 2022
Historique:
received: 11 05 2021
accepted: 27 05 2021
pubmed: 10 7 2021
medline: 1 4 2022
entrez: 9 7 2021
Statut: ppublish

Résumé

In 2011, Hanahan and Weinberg added "Deregulating Cellular Energetics" and "Avoiding Immune Destruction" to the six previous hallmarks of cancer. Since this seminal paper, there has been a growing consensus that these new hallmarks are not mutually exclusive but rather interdependent. The following review summarizes how founding genetic events for tumorigenesis ultimately increase tumor cell glycolysis, which not only supports the metabolic demands of malignancy but also provides an immunoprotective niche, promoting malignant cell proliferation, maintenance and progression. The mechanisms by which altered metabolism contributes to immune impairment are multifactorial: (1) the metabolic demands of proliferating tumor cells and activated immune cells are similar, thus creating a situation where immune cells may be in competition for key nutrients; (2) the metabolic byproducts of aerobic glycolysis directly inhibit antitumor immunity while promoting a regulatory immune phenotype; and (3) the gene programs associated with the upregulation of glycolysis also result in the generation of immunosuppressive cytokines and metabolites. From this perspective, we shed light on important considerations for the development of new classes of agents targeting cancer metabolism. These types of therapies can impair tumor growth but also pose a significant risk of stifling antitumor immunity.

Identifiants

pubmed: 34239083
doi: 10.1038/s41423-021-00727-3
pii: 10.1038/s41423-021-00727-3
pmc: PMC8752729
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

46-58

Subventions

Organisme : NCI NIH HHS
ID : F30 CA247202
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA217987
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007347
Pays : United States

Informations de copyright

© 2021. The Author(s), under exclusive licence to CSI and USTC.

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Auteurs

Bradley I Reinfeld (BI)

Department of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.

W Kimryn Rathmell (WK)

Department of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.

Tae Kon Kim (TK)

Department of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA.

Jeffrey C Rathmell (JC)

Vanderbilt Center for Immunobiology, Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA. jeff.rathmell@vumc.org.

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