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CD248 facilitates tumor growth via its cytoplasmic domain

(2011) BMC CANCER. 11.
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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
Keywords
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

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Citation

Please use this url to cite or link to this publication:

MLA
Maia, Margarida, et al. “CD248 Facilitates Tumor Growth via Its Cytoplasmic Domain.” BMC CANCER, vol. 11, 2011, doi:10.1186/1471-2407-11-162.
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. https://doi.org/10.1186/1471-2407-11-162
Chicago author-date
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. https://doi.org/10.1186/1471-2407-11-162.
Chicago author-date (all authors)
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. doi:10.1186/1471-2407-11-162.
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.
IEEE
[1]
M. Maia et al., “CD248 facilitates tumor growth via its cytoplasmic domain,” BMC CANCER, vol. 11, 2011.
@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}},
  keywords     = {{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}},
}

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