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TGFβ suppresses CD248 expression in non-cancer cells via canonical Smad-dependent signaling pathwaysTGFβ suppresses CD248 expression in non-cancer cells via canonical Smad-dependent signaling pathwaysSuresh S, Valdez Y, Xu A, O’Byrne A, Calvo F, Lei V and Conway EM. 2014-02-19T23:00:00Z<p style="text-align:justify;"><span class="ms-rteThemeForeColor-2-5 ms-rteThemeFontFace-1 ms-rteFontSize-2">​<span style="font-weight:bold;">Abstract</span></span></p><div style="color:#000000;font-family:arial, helvetica, clean, sans-serif;text-align:justify;"><h4 style="margin:0px 0.25em 0px 0px;color:#000000;font-weight:bold;text-transform:uppercase;float:left;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">BACKGROUND: </span></h4><p style="margin-bottom:0.5em;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">CD248 is a cell surface glycoprotein, highly expressed by stromal cells and fibroblasts of tumors and inflammatory lesions, but virtually undetectable in healthy adult tissues. CD248 promotes tumorigenesis, while lack of CD248 in mice confers resistance to tumor growth. Mechanisms by which CD248 is downregulated are poorly understood, hindering the development of anti-cancer therapies.</span></p><h4 style="margin:0px 0.25em 0px 0px;color:#000000;font-weight:bold;text-transform:uppercase;float:left;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">METHODS: </span></h4><p style="margin-bottom:0.5em;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">We sought to characterize the molecular mechanisms by which CD248 is downregulated by surveying its expression in different cells in response to cytokines and growth factors.</span></p><h4 style="margin:0px 0.25em 0px 0px;color:#000000;font-weight:bold;text-transform:uppercase;float:left;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">RESULTS: </span></h4><p style="margin-bottom:0.5em;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">Only transforming growth factor (TGFβ) suppressed CD248 protein and mRNA levels in cultured fibroblasts and vascular smooth muscle cells in a concentration- and time-dependent manner. TGFβ transcriptionally downregulated CD248 by signaling through canonical Smad2/3-dependent pathways, but not via mitogen activated protein kinases p38 or ERK1/2. Notably, cancer associated fibroblasts (CAF) and cancer cells were resistant to TGFβ mediated suppression of CD248.</span></p><h4 style="margin:0px 0.25em 0px 0px;color:#000000;font-weight:bold;text-transform:uppercase;float:left;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">CONCLUSIONS: </span></h4><p style="margin-bottom:0.5em;font-size:1.04em;"><span class="ms-rteThemeFontFace-1 ms-rteFontSize-2">The findings indicate that decoupling of CD248 regulation by TGFβ may contribute to its tumor-promoting properties, and underline the importance of exploring the TGFβ-CD248 signaling pathway as a potential therapeutic target for early prevention of cancer and proliferative disorders.</span><br></p></div><p><a href="https://www.ncbi.nlm.nih.gov/pubmed/24555435">​BMC Cancer 14(1):113. </a><br></p>188

 
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Instituto de Biomedicina y Biotecnología de Cantabria.
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