SOX10 Inhibits T Cell Recognition by Inducing Expression of the Immune Checkpoint Molecule PD-L1 in A375 Melanoma Cells.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Apr 2023
Historique:
received: 29 12 2022
revised: 05 01 2023
accepted: 23 01 2023
medline: 29 3 2023
entrez: 28 3 2023
pubmed: 29 3 2023
Statut: ppublish

Résumé

Malignant melanoma is a fatal skin cancer and is among the most immunogenic malignancies expressing melanoma-differentiation antigens and neoantigens. SRY-related HMG-box 10 (SOX10) is a transcription factor and a neural-crest differentiation marker that is used as a diagnostic marker for melanoma whilst playing a role in melanoma initiation through activation of the SOX10-MITF axis. SOX10 was shown to play a role in melanoma initiation by inducing expression of immune checkpoint molecules (e.g., HVEM and CEACAM1). In this study, we aimed to investigate the relationship between SOX10 and the expression an immune checkpoint molecule, programmed death-1 ligand 1 (PD-L1). SOX10 overexpression and knockdown was performed using SOX10 gene transfection and SOX10 siRNA transfection into A375 melanoma cells. PD-L1 expression was assessed by flow cytometry and western blotting. T cell response was evaluated using NY-ESO-1 specific TCR-transduced T (TCR-T) cells by IFNγ ELISPOT assay. SOX10 overexpression increased the expression of PD-L1, whereas SOX10 knockdown, using siRNA, decreased its expression. IFNγ ELISPOT assay revealed that overexpression of SOX10 decreased the susceptibility of cells to NY-ESO-1-specific TCR-T cells. SOX10 has a role in the intrinsic immune suppressive mechanisms of melanoma through expression of PD-L1.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
Malignant melanoma is a fatal skin cancer and is among the most immunogenic malignancies expressing melanoma-differentiation antigens and neoantigens. SRY-related HMG-box 10 (SOX10) is a transcription factor and a neural-crest differentiation marker that is used as a diagnostic marker for melanoma whilst playing a role in melanoma initiation through activation of the SOX10-MITF axis. SOX10 was shown to play a role in melanoma initiation by inducing expression of immune checkpoint molecules (e.g., HVEM and CEACAM1). In this study, we aimed to investigate the relationship between SOX10 and the expression an immune checkpoint molecule, programmed death-1 ligand 1 (PD-L1).
MATERIALS AND METHODS METHODS
SOX10 overexpression and knockdown was performed using SOX10 gene transfection and SOX10 siRNA transfection into A375 melanoma cells. PD-L1 expression was assessed by flow cytometry and western blotting. T cell response was evaluated using NY-ESO-1 specific TCR-transduced T (TCR-T) cells by IFNγ ELISPOT assay.
RESULTS RESULTS
SOX10 overexpression increased the expression of PD-L1, whereas SOX10 knockdown, using siRNA, decreased its expression. IFNγ ELISPOT assay revealed that overexpression of SOX10 decreased the susceptibility of cells to NY-ESO-1-specific TCR-T cells.
CONCLUSION CONCLUSIONS
SOX10 has a role in the intrinsic immune suppressive mechanisms of melanoma through expression of PD-L1.

Identifiants

pubmed: 36974807
pii: 43/4/1477
doi: 10.21873/anticanres.16296
doi:

Substances chimiques

Immune Checkpoint Proteins 0
B7-H1 Antigen 0
Ligands 0
Programmed Cell Death 1 Receptor 0
Receptors, Antigen, T-Cell 0
SOX10 protein, human 0
SOXE Transcription Factors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1477-1484

Informations de copyright

Copyright © 2023 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Kenta Sasaki (K)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Department of Dermatology, Asahikawa Medical University School of Medicine, Hokkaido, Japan.

Yoshihiko Hirohashi (Y)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan; hirohash@sapmed.ac.jp.

Kenji Murata (K)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Tomoyuki Minowa (T)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Department of Dermatology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Munehide Nakatsugawa (M)

Department of Pathology, Tokyo Medical University Hachioji Medical Center, Tokyo, Japan.

Aiko Murai (A)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Yuka Mizue (Y)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Terufumi Kubo (T)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Takayuki Kanaseki (T)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Tomohide Tsukahara (T)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Sadahiro Iwabuchi (S)

Department of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.

Shinichi Hashimoto (S)

Department of Molecular Pathophysiology, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.

Hisashi Uhara (H)

Department of Dermatology, Sapporo Medical University School of Medicine, Sapporo, Japan.

Akemi Ishida-Yamamoto (A)

Department of Dermatology, Asahikawa Medical University School of Medicine, Hokkaido, Japan.

Toshihiko Torigoe (T)

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan; torigoe@sapmed.ac.jp.

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Classifications MeSH