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CD248 facilitates tumor growth via its cytoplasmic domain

Margarida Maia, Astrid DeVriese, Tom Janssens, Michael Moons, Rik J Lories, Jan Tavernier UGent and Edward M Conway (2011) BMC CANCER. 11.
abstract
Background: Stromal fibroblasts participate in the development of a permissive environment for tumor growth, yet molecular pathways to therapeutically target fibroblasts are poorly defined. CD248, also known as endosialin or tumor endothelial marker 1 (TEM1), is a transmembrane glycoprotein expressed on activated fibroblasts. We recently showed that the cytoplasmic domain of CD248 is important in facilitating an inflammatory response in a mouse model of arthritis. Others have reported that CD248 gene inactivation in mice results in dampened tumor growth. We hypothesized that the conserved cytoplasmic domain of CD248 is important in regulating tumor growth. Methods: Mice lacking the cytoplasmic domain of CD248 (CD248(CyD/CyD)) were generated and evaluated in tumor models, comparing the findings with wild-type mice (CD248(WT/WT)). Results: As compared to the response in CD248(WT/WT) mice, growth of T241 fibrosarcomas and Lewis lung carcinomas was significantly reduced in CD248(CyD/CyD) mice. Tumor size was similar to that seen with CD248-deficient mice. Conditioned media from CD248(CyD/CyD) fibroblasts were less effective at supporting T241 fibrosarcoma cell survival. In addition to our previous observation of reduced release of activated matrix metalloproteinase (MMP)-9, CD248(CyD/CyD) fibroblasts also had impaired PDGF-BB-induced migration and expressed higher transcripts of tumor suppressor factors, transgelin (SM22 alpha), Hes and Hey1. Conclusions: The multiple pathways regulated by the cytoplasmic domain of CD248 highlight its potential as a therapeutic target to treat cancer. Keywords: stromal fibroblast suppressor, transgenic, endosialin, tumor endothelial marker
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
tumor endothelial marker, transgenic, endosialin, stromal fibroblast suppressor, IN-VITRO, MURAL CELLS, BRAIN-TUMORS, STROMAL FIBROBLASTS, THERAPEUTIC TARGET, COLORECTAL-CANCER, ENDOSIALIN TEM1, ENDOTHELIAL MARKERS, LECTIN-LIKE DOMAIN, CANCER-ASSOCIATED FIBROBLASTS
journal title
BMC CANCER
BMC Cancer
volume
11
article_number
162
pages
12 pages
Web of Science type
Article
Web of Science id
000291261000001
JCR category
ONCOLOGY
JCR impact factor
3.011 (2011)
JCR rank
77/190 (2011)
JCR quartile
2 (2011)
ISSN
1471-2407
DOI
10.1186/1471-2407-11-162
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1851293
handle
http://hdl.handle.net/1854/LU-1851293
date created
2011-07-01 15:34:27
date last changed
2013-01-30 09:41:13
@article{1851293,
  abstract     = {Background: Stromal fibroblasts participate in the development of a permissive environment for tumor growth, yet molecular pathways to therapeutically target fibroblasts are poorly defined. CD248, also known as endosialin or tumor endothelial marker 1 (TEM1), is a transmembrane glycoprotein expressed on activated fibroblasts. We recently showed that the cytoplasmic domain of CD248 is important in facilitating an inflammatory response in a mouse model of arthritis. Others have reported that CD248 gene inactivation in mice results in dampened tumor growth. We hypothesized that the conserved cytoplasmic domain of CD248 is important in regulating tumor growth. Methods: Mice lacking the cytoplasmic domain of CD248 (CD248(CyD/CyD)) were generated and evaluated in tumor models, comparing the findings with wild-type mice (CD248(WT/WT)). Results: As compared to the response in CD248(WT/WT) mice, growth of T241 fibrosarcomas and Lewis lung carcinomas was significantly reduced in CD248(CyD/CyD) mice. Tumor size was similar to that seen with CD248-deficient mice. Conditioned media from CD248(CyD/CyD) fibroblasts were less effective at supporting T241 fibrosarcoma cell survival. In addition to our previous observation of reduced release of activated matrix metalloproteinase (MMP)-9, CD248(CyD/CyD) fibroblasts also had impaired PDGF-BB-induced migration and expressed higher transcripts of tumor suppressor factors, transgelin (SM22 alpha), Hes and Hey1. Conclusions: The multiple pathways regulated by the cytoplasmic domain of CD248 highlight its potential as a therapeutic target to treat cancer. Keywords: stromal fibroblast suppressor, transgenic, endosialin, tumor endothelial marker},
  articleno    = {162},
  author       = {Maia, Margarida and DeVriese, Astrid and Janssens, Tom and Moons, Michael and Lories, Rik J and Tavernier, Jan and Conway, Edward M},
  issn         = {1471-2407},
  journal      = {BMC CANCER},
  keyword      = {tumor endothelial marker,transgenic,endosialin,stromal fibroblast suppressor,IN-VITRO,MURAL CELLS,BRAIN-TUMORS,STROMAL FIBROBLASTS,THERAPEUTIC TARGET,COLORECTAL-CANCER,ENDOSIALIN TEM1,ENDOTHELIAL MARKERS,LECTIN-LIKE DOMAIN,CANCER-ASSOCIATED FIBROBLASTS},
  language     = {eng},
  pages        = {12},
  title        = {CD248 facilitates tumor growth via its cytoplasmic domain},
  url          = {http://dx.doi.org/10.1186/1471-2407-11-162},
  volume       = {11},
  year         = {2011},
}

Chicago
Maia, Margarida, Astrid DeVriese, Tom Janssens, Michael Moons, Rik J Lories, Jan Tavernier, and Edward M Conway. 2011. “CD248 Facilitates Tumor Growth via Its Cytoplasmic Domain.” Bmc Cancer 11.
APA
Maia, M., DeVriese, A., Janssens, T., Moons, M., Lories, R. J., Tavernier, J., & Conway, E. M. (2011). CD248 facilitates tumor growth via its cytoplasmic domain. BMC CANCER, 11.
Vancouver
1.
Maia M, DeVriese A, Janssens T, Moons M, Lories RJ, Tavernier J, et al. CD248 facilitates tumor growth via its cytoplasmic domain. BMC CANCER. 2011;11.
MLA
Maia, Margarida, Astrid DeVriese, Tom Janssens, et al. “CD248 Facilitates Tumor Growth via Its Cytoplasmic Domain.” BMC CANCER 11 (2011): n. pag. Print.