Journal
CANCER CELL
Volume 30, Issue 1, Pages 147-160Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.05.016
Keywords
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Funding
- Ligue Nationale contre le Cancer
- Site de Recherche Integree sur le Cancer (IRIC) Socrates
- ISREC Foundation
- Agence Nationale pour la Recherche (ANR AUTOPH)
- Agence Nationale pour la Recherche (ANR Emergence)
- European Commission (ArtForce)
- European Research Council
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Fondation de France
- Canceropole Ile-de-France
- Fondation Bettencourt-Schueller
- LabEx Immuno-Oncology
- Paris Alliance of Cancer Research Institutes
- EU
- ERC
- Era of Hope/DoD Innovator Award
- FWF [I1000, P23490-B12, P24381-B20]
- BMWFW
- AIRC [IG5354]
- Telethon [GGP06070]
- ERA-NET Neuron Nanostroke
- Ministry of Health of Italy [RF-2011-02348435]
- Italian Ministry of Education, University and Research [RBAP11FXBC_001]
- University of Ferrara
- NIH [RO1CA109618, U19 AI109725]
- Cancer Prevention and Research Institute of Texas [RP120718]
- Austrian Science Fund (FWF) [P27893] Funding Source: Austrian Science Fund (FWF)
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Caloric restriction mimetics (CRMs) mimic the biochemical effects of nutrient deprivation by reducing lysine acetylation of cellular proteins, thus triggering autophagy. Treatment with the CRM hydroxycitrate, an inhibitor of ATP citrate lyase, induced the depletion of regulatory T cells (which dampen anticancer immunity) from autophagy-competent, but not autophagy-deficient, mutant KRAS-induced lung cancers in mice, thereby improving anticancer immunosurveillance and reducing tumor mass. Short-term fasting or treatment with several chemically unrelated autophagy-inducing CRMs, including hydroxycitrate and spermidine, improved the inhibition of tumor growth by chemotherapy in vivo. This effect was only observed for autophagy-competent tumors, depended on the presence of T lymphocytes, and was accompanied by the depletion of regulatory T cells from the tumor bed.
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