ERRα Expression in Bone Metastases Leads to an Exacerbated Antitumor Immune Response.
Animals
Apoptosis
Biomarkers, Tumor
/ genetics
Bone Neoplasms
/ immunology
Breast Neoplasms
/ immunology
Cell Proliferation
Chemokine CCL17
/ genetics
Chemokine CCL20
/ genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Mice
Mice, Inbred BALB C
Mice, Nude
Prognosis
Receptors, Estrogen
/ genetics
Signal Transduction
T-Lymphocytes
/ immunology
Transforming Growth Factor beta3
/ genetics
Tumor Cells, Cultured
Tumor Microenvironment
/ immunology
Xenograft Model Antitumor Assays
ERRalpha Estrogen-Related Receptor
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
received:
13
11
2019
revised:
20
03
2020
accepted:
28
04
2020
pubmed:
6
5
2020
medline:
18
11
2020
entrez:
6
5
2020
Statut:
ppublish
Résumé
Bone is the most common metastatic site for breast cancer. Although the estrogen-related receptor alpha (ERRα) has been implicated in breast cancer cell dissemination to the bone from the primary tumor, its role after tumor cell anchorage in the bone microenvironment remains elusive. Here, we reveal that ERRα inhibits the progression of bone metastases of breast cancer cells by increasing the immune activity of the bone microenvironment. Overexpression of ERRα in breast cancer bone metastases induced expression of chemokines CCL17 and CCL20 and repressed production of TGFβ3. Subsequently, CD8
Identifiants
pubmed: 32366476
pii: 0008-5472.CAN-19-3584
doi: 10.1158/0008-5472.CAN-19-3584
doi:
Substances chimiques
Biomarkers, Tumor
0
CCL17 protein, human
0
CCL20 protein, human
0
Chemokine CCL17
0
Chemokine CCL20
0
Receptors, Estrogen
0
TGFB3 protein, human
0
Transforming Growth Factor beta3
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2914-2926Informations de copyright
©2020 American Association for Cancer Research.