Blockade of β-Catenin-Induced CCL28 Suppresses Gastric Cancer Progression via Inhibition of Treg Cell Infiltration.
Adenocarcinoma
/ immunology
Animals
Chemokines, CC
/ immunology
Disease Progression
Gene Expression Regulation, Neoplastic
/ physiology
Humans
Lymphocytes, Tumor-Infiltrating
/ immunology
Mice
Stomach Neoplasms
/ immunology
T-Lymphocytes, Regulatory
/ immunology
Tumor Escape
/ physiology
Tumor Microenvironment
/ immunology
beta Catenin
/ immunology
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
15 05 2020
15 05 2020
Historique:
received:
02
10
2019
revised:
07
01
2020
accepted:
05
03
2020
pubmed:
12
3
2020
medline:
27
10
2020
entrez:
12
3
2020
Statut:
ppublish
Résumé
Dysregulation of Wnt/β-catenin signaling is frequently observed in human gastric cancer. Elucidation of the tumor immune microenvironment is essential for understanding tumorigenesis and for the development of immunotherapeutic strategies. However, it remains unclear how β-catenin signaling regulates the tumor immune microenvironment in the stomach. Here, we identify CCL28 as a direct transcriptional target gene of β-catenin/T-cell factor (TCF). Protein levels of β-catenin and CCL28 positively correlated in human gastric adenocarcinoma. β-Catenin-activated CCL28 recruited regulatory T (Treg) cells in a transwell migration assay. In a clinically relevant mouse gastric cancer model established by
Identifiants
pubmed: 32156780
pii: 0008-5472.CAN-19-3074
doi: 10.1158/0008-5472.CAN-19-3074
doi:
Substances chimiques
CCL28 protein, human
0
Chemokines, CC
0
beta Catenin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2004-2016Informations de copyright
©2020 American Association for Cancer Research.