Immune Evasion Mechanism and AXL

Extensive interest in cancer immunotherapy is reported according to the clinical importance of CTLA-4 and (PD-1/PD-L1) [programmed death (PD) and programmed death-ligand (PD-L1)] in immune checkpoint therapies. AXL is a receptor tyrosine kinase expressed in different types of cancer and in relation...

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Main Authors: Hye-Youn Son, Hwan-Kyu Jeong
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-10-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2021.756225/full
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author Hye-Youn Son
Hwan-Kyu Jeong
author_facet Hye-Youn Son
Hwan-Kyu Jeong
author_sort Hye-Youn Son
collection DOAJ
description Extensive interest in cancer immunotherapy is reported according to the clinical importance of CTLA-4 and (PD-1/PD-L1) [programmed death (PD) and programmed death-ligand (PD-L1)] in immune checkpoint therapies. AXL is a receptor tyrosine kinase expressed in different types of cancer and in relation to resistance against various anticancer therapeutics due to poor clinical prognosis. AXL and its ligand, i.e., growth arrest-specific 6 (GAS6) proteins, are expressed on many cancer cells, and the GAS6/AXL pathway is reported to promote cancer cell proliferation, survival, migration, invasion, angiogenesis, and immune evasion. AXL is an attractive and novel therapeutic target for impairing tumor progression from immune cell contracts in the tumor microenvironment. The GAS6/AXL pathway is also of interest immunologically because it targets fewer antitumor immune responses. In effect, several targeted therapies are selective and nonselective for AXL, which are in preclinical and clinical development in multiple cancer types. Therefore, this review focuses on the role of the GAS6/AXL signaling pathway in triggering the immunosuppressive tumor microenvironment as immune evasion. This includes regulating its composition and activating T-cell exclusion with the immune-suppressive activity of regulatory T cells, which is related to one of the hallmarks of cancer survival. Finally, this article discusses the GAS6/AXL signaling pathway in the context of several immune responses such as NK cell activation, apoptosis, and tumor-specific immunity, especially PD-1/PDL-1 signaling.
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spelling doaj.art-29e31181f2b74026b6953527f80156a42022-12-21T21:47:53ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2021-10-011110.3389/fonc.2021.756225756225Immune Evasion Mechanism and AXLHye-Youn Son0Hwan-Kyu Jeong1Department of Breast and Endocrine Surgery, Center for Medical Innovation, Seoul National University Hospital, Seoul, South KoreaSchool of Biosystems and Biomedical Sciences, Korea University, Seoul, South KoreaExtensive interest in cancer immunotherapy is reported according to the clinical importance of CTLA-4 and (PD-1/PD-L1) [programmed death (PD) and programmed death-ligand (PD-L1)] in immune checkpoint therapies. AXL is a receptor tyrosine kinase expressed in different types of cancer and in relation to resistance against various anticancer therapeutics due to poor clinical prognosis. AXL and its ligand, i.e., growth arrest-specific 6 (GAS6) proteins, are expressed on many cancer cells, and the GAS6/AXL pathway is reported to promote cancer cell proliferation, survival, migration, invasion, angiogenesis, and immune evasion. AXL is an attractive and novel therapeutic target for impairing tumor progression from immune cell contracts in the tumor microenvironment. The GAS6/AXL pathway is also of interest immunologically because it targets fewer antitumor immune responses. In effect, several targeted therapies are selective and nonselective for AXL, which are in preclinical and clinical development in multiple cancer types. Therefore, this review focuses on the role of the GAS6/AXL signaling pathway in triggering the immunosuppressive tumor microenvironment as immune evasion. This includes regulating its composition and activating T-cell exclusion with the immune-suppressive activity of regulatory T cells, which is related to one of the hallmarks of cancer survival. Finally, this article discusses the GAS6/AXL signaling pathway in the context of several immune responses such as NK cell activation, apoptosis, and tumor-specific immunity, especially PD-1/PDL-1 signaling.https://www.frontiersin.org/articles/10.3389/fonc.2021.756225/fullPD-1/PD-L1Gas6/Axl signalingimmune checkpointimmune evasiontumor microenvironment (TME)AXL
spellingShingle Hye-Youn Son
Hwan-Kyu Jeong
Immune Evasion Mechanism and AXL
Frontiers in Oncology
PD-1/PD-L1
Gas6/Axl signaling
immune checkpoint
immune evasion
tumor microenvironment (TME)
AXL
title Immune Evasion Mechanism and AXL
title_full Immune Evasion Mechanism and AXL
title_fullStr Immune Evasion Mechanism and AXL
title_full_unstemmed Immune Evasion Mechanism and AXL
title_short Immune Evasion Mechanism and AXL
title_sort immune evasion mechanism and axl
topic PD-1/PD-L1
Gas6/Axl signaling
immune checkpoint
immune evasion
tumor microenvironment (TME)
AXL
url https://www.frontiersin.org/articles/10.3389/fonc.2021.756225/full
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