Mitochondrial metabolism: Inducer or therapeutic target in tumor immune-resistance?

Animals Antineoplastic Agents / pharmacology Drug Resistance, Neoplasm / drug effects Humans Mitochondria / drug effects Neoplasms / drug therapy
Immunogenic cell death Mitochondrial danger-associated molecular patterns Mitochondrial metabolism Tumor-induced immune-escape Tumor-induced immune-suppression

Journal

Seminars in cell & developmental biology
ISSN: 1096-3634
Titre abrégé: Semin Cell Dev Biol
Pays: England
ID NLM: 9607332

Informations de publication

Date de publication:
02 2020
Historique:
received: 28 03 2019
revised: 09 05 2019
accepted: 10 05 2019
pubmed: 18 5 2019
medline: 23 12 2020
entrez: 18 5 2019
Statut: ppublish

Résumé

Mitochondria have been considered for a long time only as the principal source of building blocks and energy upon aerobic conditions. Recently they emerged as key players in cell proliferation, invasion and resistance to therapy. The most aggressive tumors are able to evade the immune-surveillance. Alterations in the mitochondria metabolism either in cancer cells or in host immune system cells are involved in such tumor-induced immune-suppression. This review will focus on the main mitochondrial dysfunctions in tumor and immune cell populations determining immune-resistance, and on the therapies that may target mitochondrial metabolism and restore a powerful anti-tumor immune-activity.

Identifiants

DOI: 10.1016/j.semcdb.2019.05.008 PMID: 31100351
pubmed: 31100351
pii: S1084-9521(18)30164-2
doi: 10.1016/j.semcdb.2019.05.008
pii:
doi:

Substances chimiques

Antineoplastic Agents 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

80-89

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Joanna Kopecka (J)

Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy.

Elena Gazzano (E)

Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy.

Barbara Castella (B)

Laboratory of Blood Tumor Immunology, Department of Molecular Biotechnology and Health Sciences, University of Torino, Italy.

Iris C Salaroglio (IC)

Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy.

Eleonora Mungo (E)

Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy.

Massimo Massaia (M)

Laboratory of Blood Tumor Immunology, Department of Molecular Biotechnology and Health Sciences, University of Torino, Italy; Hematology Division, AO S Croce e Carle, Cuneo, Italy; Interdepartmental Center of Research in Molecular Biotechnology, University of Torino, Italy.

Chiara Riganti (C)

Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy; Interdepartmental Center of Research in Molecular Biotechnology, University of Torino, Italy. Electronic address: chiara.riganti@unito.it.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Mitochondrial metabolism: Inducer or...
questionsmedicales.fr › Actions chimiques et utilisations › Actions pharmacologiques › Utilisations thérapeutiques › Antinéoplasiques › Mitochondrial metabolism: Inducer or...
questionsmedicales.fr › Phénomènes physiologiques › Phénomènes pharmacologiques et toxicologiques › Phénomènes pharmacologiques › Résistance aux substances › Résistance aux médicaments antinéoplasiques › Mitochondrial metabolism: Inducer or...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › Mitochondrial metabolism: Inducer or...
questionsmedicales.fr › Cellules › Structures cellulaires › Fractions subcellulaires › Mitochondries › Mitochondrial metabolism: Inducer or...
questionsmedicales.fr › Tumeurs › Mitochondrial metabolism: Inducer or...