Inhibition of vascular adhesion protein-1 enhances the anti-tumor effects of immune checkpoint inhibitors.


Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
Apr 2021
Historique:
revised: 10 01 2021
received: 20 06 2020
accepted: 12 01 2021
pubmed: 17 1 2021
medline: 10 4 2021
entrez: 16 1 2021
Statut: ppublish

Résumé

Modulation of the immunosuppressive tumor microenvironment (TME) is essential for enhancing the anti-tumor effects of immune checkpoint inhibitors (ICIs). Adhesion molecules and enzymes such as vascular adhesion protein-1 (VAP-1), which are expressed in some cancers and tumor vascular endothelial cells, may be involved in the generation of an immunosuppressive TME. In this study, the role of VAP-1 in TME was investigated in 2 murine colon cancer models and human cancer cells. Intraperitoneal administration of the VAP-1-specific inhibitor U-V296 inhibited murine tumor growth by enhancing IFN-γ-producing tumor antigen-specific CD8

Identifiants

pubmed: 33453147
doi: 10.1111/cas.14812
pmc: PMC8019209
doi:

Substances chimiques

Cell Adhesion Molecules 0
Immune Checkpoint Inhibitors 0
Amine Oxidase (Copper-Containing) EC 1.4.3.21
semicarbazide-sensitive amine oxidase-vascular adhesion protein-1, mouse EC 1.4.3.21

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1390-1401

Subventions

Organisme : Japan Agency for Medical Research and Development
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 15K09783
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 19K16808
Organisme : Ministry of Education, Culture, Sports, Science and Technology
ID : 26221005

Informations de copyright

© 2021 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Tomonari Kinoshita (T)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Division of General Thoracic Surgery, Department of Surgery, Keio University School of Medicine, Tokyo, Japan.

Mohammad Abu Sayem (MA)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Department of Biotechnology and Genetic Engineering, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.

Tomonori Yaguchi (T)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.

Budiman Kharma (B)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.

Kenji Morii (K)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.

Daiki Kato (D)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Laboratory of Veterinary Surgery, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.

Shigeki Ohta (S)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.

Yukihiko Mashima (Y)

Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.

Hisao Asamura (H)

Division of General Thoracic Surgery, Department of Surgery, Keio University School of Medicine, Tokyo, Japan.

Yutaka Kawakami (Y)

Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Department of Immunology, School of Medicine, International University of Health and Welfare, Chiba, Japan.

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Classifications MeSH