Energy status dictates PD-L1 protein abundance and anti-tumor immunity to enable checkpoint blockade.


Journal

Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571

Informations de publication

Date de publication:
03 06 2021
Historique:
received: 01 04 2020
revised: 26 10 2020
accepted: 22 03 2021
pubmed: 29 4 2021
medline: 23 6 2021
entrez: 28 4 2021
Statut: ppublish

Résumé

Aberrant energy status contributes to multiple metabolic diseases, including obesity, diabetes, and cancer, but the underlying mechanism remains elusive. Here, we report that ketogenic-diet-induced changes in energy status enhance the efficacy of anti-CTLA-4 immunotherapy by decreasing PD-L1 protein levels and increasing expression of type-I interferon (IFN) and antigen presentation genes. Mechanistically, energy deprivation activates AMP-activated protein kinase (AMPK), which in turn, phosphorylates PD-L1 on Ser283, thereby disrupting its interaction with CMTM4 and subsequently triggering PD-L1 degradation. In addition, AMPK phosphorylates EZH2, which disrupts PRC2 function, leading to enhanced IFNs and antigen presentation gene expression. Through these mechanisms, AMPK agonists or ketogenic diets enhance the efficacy of anti-CTLA-4 immunotherapy and improve the overall survival rate in syngeneic mouse tumor models. Our findings reveal a pivotal role for AMPK in regulating the immune response to immune-checkpoint blockade and advocate for combining ketogenic diets or AMPK agonists with anti-CTLA4 immunotherapy to combat cancer.

Identifiants

pubmed: 33909988
pii: S1097-2765(21)00232-X
doi: 10.1016/j.molcel.2021.03.037
pmc: PMC8178223
mid: NIHMS1690825
pii:
doi:

Substances chimiques

Antibodies, Neutralizing 0
Antineoplastic Agents 0
B7-H1 Antigen 0
Biphenyl Compounds 0
CMTM4 protein, mouse 0
CTLA-4 Antigen 0
Cd274 protein, mouse 0
Ctla4 protein, mouse 0
Immune Checkpoint Inhibitors 0
MARVEL Domain-Containing Proteins 0
Pyrones 0
Thiophenes 0
Enhancer of Zeste Homolog 2 Protein EC 2.1.1.43
Ezh2 protein, mouse EC 2.1.1.43
AMPK alpha1 subunit, mouse EC 2.7.11.1
AMP-Activated Protein Kinases EC 2.7.11.31
4-hydroxy-3-(4-(2-hydroxyphenyl)phenyl)-6-oxo-7H-thieno(2,3-b)pyridine-5-carbonitrile P68477CD2C

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

2317-2331.e6

Subventions

Organisme : NCI NIH HHS
ID : K99 CA259329
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA206963
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA101942
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM094777
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA177910
Pays : United States
Organisme : NCI NIH HHS
ID : R35 CA253027
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests G.J.F. has patents/pending royalties on the PD-1 pathway from Roche, Merck, Bristol-Myers-Squibb, EMD-Serono, Boehringer-Ingelheim, AstraZeneca, Dako, and Novartis. G.J.F. has served on advisory boards for Roche, Bristol-Myers-Squibb, Xios, Origimed, Triursus, iTeos, NextPoint, IgM, Jubilant, Geode, and GV20. G.J.F. has equity in Nextpoint, Triursus, Xios, iTeos, IgM, Geode, and GV20. W.W. is a co-founder and consultant for ReKindle Therapeutics. The other authors declare no competing interests.

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Auteurs

Xiaoming Dai (X)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Xia Bu (X)

Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.

Yang Gao (Y)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA; Department of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.

Jianping Guo (J)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Jia Hu (J)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Cong Jiang (C)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Zhao Zhang (Z)

Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.

Kexin Xu (K)

Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.

Jinzhi Duan (J)

Division of Gastroenterology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Shaohui He (S)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Jinfang Zhang (J)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.

Lixin Wan (L)

Department of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.

Tianjie Liu (T)

Department of Urology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.

Xiaobo Zhou (X)

Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Mien-Chie Hung (MC)

Graduate Institute of Biomedical Sciences and Center for Molecular Medicine, China Medical University, Taichung 404, Taiwan.

Gordon J Freeman (GJ)

Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: gordon_freeman@dfci.harvard.edu.

Wenyi Wei (W)

Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. Electronic address: wwei2@bidmc.harvard.edu.

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Classifications MeSH