期刊
CELL METABOLISM
卷 27, 期 4, 页码 828-+出版社
CELL PRESS
DOI: 10.1016/j.cmet.2018.02.009
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资金
- Fondation ARC pour la Recherche sur le Cancer
- Agence Nationale de la Recherche [LABEX SIGNALIFE ANR-11-LABX-0028-01]
- Inserm
- Canceropole PACA
- Institut National du Cancer
- Conseil Regional PACA
- CEA
- French Ministry of Research
- National Research Agency as part of the French metabolomics and fluxomics infrastructure (MetaboHUB) [ANR-11-INBS-0010]
- la Fondation pour la Recherche Medicale (FRM)
- La Ligue contre le Cancer
- Institut National Du Cancer [INCa PLBIO: 2015-111, INCA-7981]
- Ligue Contre le Cancer (Comite des Landes, LARGE project)
- EU [H2020MSCAITN-675448]
- Societe Francophone du Diabete
- Association Francaise pour l'Etude du Foie (AFEF)/Aptalis
- Fondation ARC
Dietary restriction (DR) was shown to impact on tumor growth with very variable effects depending on the cancer type. However, how DR limits cancer progression remains largely unknown. Here, we demonstrate that feeding mice a low-protein (Low PROT) isocaloric diet but not a low-carbohydrate (Low CHO) diet reduced tumor growth in three independent mouse cancer models. Surprisingly, this effect relies on anticancer immunosurveillance, as depleting CD8(+) T cells, antigen-presenting cells (APCs), or using immunodeficient mice prevented the beneficial effect of the diet. Mechanistically, we established that a Low PROT diet induces the unfolded protein response (UPR) in tumor cells through the activation of IRE1 alpha and RIG1 signaling, thereby resulting in cytokine production and mounting an efficient anticancer immune response. Collectively, our data suggest that a Low PROT diet induces an IRE1 alpha-dependent UPR in cancer cells, enhancing a CD8-mediated T cell response against tumors.
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