SOX10 requirement for melanoma tumor growth is due, in part, to immune-mediated effects.
Animals
Antigens, CD
/ genetics
CD8-Positive T-Lymphocytes
/ immunology
Carcinoembryonic Antigen
/ genetics
Cell Adhesion Molecules
/ genetics
Cell Line, Tumor
Cell Proliferation
Databases, Genetic
Gene Expression Regulation, Neoplastic
Humans
Lymphocytes, Tumor-Infiltrating
/ immunology
Male
Melanoma
/ genetics
Mice, Inbred C57BL
Mice, Inbred NOD
Mice, SCID
Receptors, Tumor Necrosis Factor, Member 14
/ genetics
SOXE Transcription Factors
/ genetics
Signal Transduction
Skin Neoplasms
/ genetics
Tumor Burden
CEACAM1
HVEM
SOX10
de-differentiation
immune checkpoint
melanoma
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
07 12 2021
07 12 2021
Historique:
received:
12
01
2021
revised:
28
09
2021
accepted:
10
11
2021
entrez:
8
12
2021
pubmed:
9
12
2021
medline:
15
2
2022
Statut:
ppublish
Résumé
Developmental factors may regulate the expression of immune modulatory proteins in cancer, linking embryonic development and cancer cell immune evasion. This is particularly relevant in melanoma because immune checkpoint inhibitors are commonly used in the clinic. SRY-box transcription factor 10 (SOX10) mediates neural crest development and is required for melanoma cell growth. In this study, we investigate immune-related targets of SOX10 and observe positive regulation of herpesvirus entry mediator (HVEM) and carcinoembryonic-antigen cell-adhesion molecule 1 (CEACAM1). Sox10 knockout reduces tumor growth in vivo, and this effect is exacerbated in immune-competent models. Modulation of CEACAM1 expression but not HVEM elicits modest effects on tumor growth. Importantly, Sox10 knockout effects on tumor growth are dependent, in part, on CD8+ T cells. Extending this analysis to samples from patients with cutaneous melanoma, we observe a negative correlation with SOX10 and immune-related pathways. These data demonstrate a role for SOX10 in regulating immune checkpoint protein expression and anti-tumor immunity in melanoma.
Identifiants
pubmed: 34879275
pii: S2211-1247(21)01576-X
doi: 10.1016/j.celrep.2021.110085
pmc: PMC8720266
mid: NIHMS1762845
pii:
doi:
Substances chimiques
Antigens, CD
0
CD66 antigens
0
Carcinoembryonic Antigen
0
Ceacam1 protein, mouse
0
Cell Adhesion Molecules
0
Receptors, Tumor Necrosis Factor, Member 14
0
SOX10 protein, human
0
SOXE Transcription Factors
0
Sox10 protein, mouse
0
TNFRSF14 protein, human
0
Tnfrsf14 protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
110085Subventions
Organisme : NIGMS NIH HHS
ID : T32 GM100836
Pays : United States
Organisme : NCI NIH HHS
ID : K00 CA245552
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA182635
Pays : United States
Organisme : NCI NIH HHS
ID : F99 CA245552
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA160495
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA056036
Pays : United States
Informations de copyright
Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests A.E.A. reports receiving a commercial research grant from Pfizer Inc. (2013–2017) and has ownership interest in patent number 9880150. No potential conflicts of interest were disclosed by the other authors.
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