CXCL17-derived CD11b
Animals
Becaplermin
/ metabolism
Breast Neoplasms
/ blood
CD11b Antigen
/ metabolism
Cell Line, Tumor
Chemokines
/ blood
Chemokines, CXC
/ metabolism
Chemotaxis
Datasets as Topic
Female
Humans
Kaplan-Meier Estimate
Lung
/ pathology
Lung Neoplasms
/ pathology
Mice
Mice, Nude
Myeloid-Derived Suppressor Cells
/ immunology
Prognosis
Receptors, Chemokine
/ metabolism
Xenograft Model Antitumor Assays
Breast cancer
CXCL17
Lung metastasis
Myeloid-derived suppressor cells
PDGF-BB
Journal
Breast cancer research : BCR
ISSN: 1465-542X
Titre abrégé: Breast Cancer Res
Pays: England
ID NLM: 100927353
Informations de publication
Date de publication:
12 02 2019
12 02 2019
Historique:
received:
26
07
2018
accepted:
01
02
2019
entrez:
14
2
2019
pubmed:
14
2
2019
medline:
23
7
2019
Statut:
epublish
Résumé
Metastasis is the major cause of death from breast cancer. Colonization and adaption of metastatic cells in distant organs is a rate-limiting step of the cancer spreading. The underlying mechanisms responsible for the colonization of breast cancer to lung metastatic niches are not fully understood. Specific gene contributions to lung metastasis were identified by comparing gene profiles of 4T1 tumors metastasizing to various organs via microarray. The oncogenic properties CXCL17 were examined by in vivo spontaneous metastasis mouse model. The chemotactic activity of CXCL17 on CD11b Here, we demonstrate that breast cancer cells secrete CXCL17, which increases the accumulation of CD11b Our study reveals that MDSCs derived by CXCL17 contribute to the establishment of a lung metastatic niche by PDGF-BB secretion and provide a rationale for development of CXCL17 or PDGF-BB antagonists to inhibit or prevent lung metastasis in cases of breast cancer.
Sections du résumé
BACKGROUND
Metastasis is the major cause of death from breast cancer. Colonization and adaption of metastatic cells in distant organs is a rate-limiting step of the cancer spreading. The underlying mechanisms responsible for the colonization of breast cancer to lung metastatic niches are not fully understood.
METHODS
Specific gene contributions to lung metastasis were identified by comparing gene profiles of 4T1 tumors metastasizing to various organs via microarray. The oncogenic properties CXCL17 were examined by in vivo spontaneous metastasis mouse model. The chemotactic activity of CXCL17 on CD11b
RESULTS
Here, we demonstrate that breast cancer cells secrete CXCL17, which increases the accumulation of CD11b
CONCLUSION
Our study reveals that MDSCs derived by CXCL17 contribute to the establishment of a lung metastatic niche by PDGF-BB secretion and provide a rationale for development of CXCL17 or PDGF-BB antagonists to inhibit or prevent lung metastasis in cases of breast cancer.
Identifiants
pubmed: 30755260
doi: 10.1186/s13058-019-1114-3
pii: 10.1186/s13058-019-1114-3
pmc: PMC6373011
doi:
Substances chimiques
CD11b Antigen
0
CXCL17 protein, human
0
CXCL17 protein, mouse
0
Chemokines
0
Chemokines, CXC
0
Gr-1 protein, mouse
0
Receptors, Chemokine
0
Becaplermin
1B56C968OA
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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