Retinoblastoma Inactivation Induces a Protumoral Microenvironment via Enhanced CCL2 Secretion.
Animals
Breast Neoplasms
/ metabolism
Cell Culture Techniques
Cell Line, Tumor
Chemokine CCL2
/ biosynthesis
Female
Gene Expression Profiling
/ methods
Humans
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, CCR2
/ metabolism
Retinoblastoma Protein
/ deficiency
Soft Tissue Neoplasms
/ metabolism
Tumor Microenvironment
Up-Regulation
Journal
Cancer research
ISSN: 1538-7445
Titre abrégé: Cancer Res
Pays: United States
ID NLM: 2984705R
Informations de publication
Date de publication:
01 08 2019
01 08 2019
Historique:
received:
19
11
2018
revised:
27
04
2019
accepted:
07
06
2019
pubmed:
14
6
2019
medline:
16
4
2020
entrez:
14
6
2019
Statut:
ppublish
Résumé
Cancer cell-intrinsic properties caused by oncogenic mutations have been well characterized; however, how specific oncogenes and tumor suppressors impact the tumor microenvironment (TME) is not well understood. Here, we present a novel non-cell-autonomous function of the retinoblastoma (RB) tumor suppressor in controlling the TME. RB inactivation stimulated tumor growth and neoangiogenesis in a syngeneic and orthotropic murine soft-tissue sarcoma model, which was associated with recruitment of tumor-associated macrophages (TAM) and immunosuppressive cells such as Gr1
Identifiants
pubmed: 31189648
pii: 0008-5472.CAN-18-3604
doi: 10.1158/0008-5472.CAN-18-3604
doi:
Substances chimiques
CCL2 protein, human
0
CCR2 protein, human
0
Ccl2 protein, mouse
0
Ccr2 protein, mouse
0
Chemokine CCL2
0
Receptors, CCR2
0
Retinoblastoma Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3903-3915Informations de copyright
©2019 American Association for Cancer Research.