Tenascin-C Orchestrates an Immune-Suppressive Tumor Microenvironment in Oral Squamous Cell Carcinoma.
Animals
Chemokine CCL21
/ immunology
Humans
Mice
Mice, Inbred C57BL
Mice, Knockout
Mouth Neoplasms
/ immunology
Receptors, CCR7
/ immunology
Recombinant Proteins
/ pharmacology
Squamous Cell Carcinoma of Head and Neck
/ immunology
T-Lymphocytes, Regulatory
/ immunology
Tenascin
/ immunology
Tumor Microenvironment
/ immunology
Journal
Cancer immunology research
ISSN: 2326-6074
Titre abrégé: Cancer Immunol Res
Pays: United States
ID NLM: 101614637
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
25
01
2020
revised:
19
04
2020
accepted:
01
07
2020
pubmed:
16
7
2020
medline:
26
8
2021
entrez:
16
7
2020
Statut:
ppublish
Résumé
Inherent immune suppression represents a major challenge in the treatment of human cancer. The extracellular matrix molecule tenascin-C promotes cancer by multiple mechanisms, yet the roles of tenascin-C in tumor immunity are incompletely understood. Using a 4NQO-induced oral squamous cell carcinoma (OSCC) model with abundant and absent tenascin-C, we demonstrated that tenascin-C enforced an immune-suppressive lymphoid stroma via CCL21/CCR7 signaling, leading to increased metastatic tumors. Through TLR4, tenascin-C increased expression of CCR7 in CD11c
Identifiants
pubmed: 32665262
pii: 2326-6066.CIR-20-0074
doi: 10.1158/2326-6066.CIR-20-0074
doi:
Substances chimiques
CCL21 protein, human
0
CCR7 protein, human
0
Chemokine CCL21
0
Receptors, CCR7
0
Recombinant Proteins
0
TNC protein, human
0
Tenascin
0
Tnc protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1122-1138Informations de copyright
©2020 American Association for Cancer Research.