کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2151447 | 1089993 | 2013 | 22 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
PDGFRB Promotes Liver Metastasis Formation of Mesenchymal-Like Colorectal Tumor Cells
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کلمات کلیدی
ECMPDGFFCSHRATRAPDAPIDFSGFPPDGFRTGFBREGFR4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولdisease-free survival - بقاء بدون بیماریoverall survival - بقای کلtransforming growth factor beta receptor - تبدیل کننده گیرنده بتا عامل رشدEMT - تکنسین فوریتهای پزشکیColorectal cancer - سرطان روده بزرگfetal calf serum - سرم گوساله جنینplatelet-derived growth factor - فاکتور رشد حاصل از پلاکتExtracellular matrix - ماتریکس خارج سلولیgreen fluorescent protein - پروتئین فلورسنت سبزCRP - پروتئین واکنشی سی یا سی. آر. پی Thrombin receptor-activating peptide - پپتید فعال گیرنده ترومبینCRC - کد افزونگی دورهای epithelial-to-mesenchymal transition - گذار اپیتلیال به مزانشیمالplatelet-derived growth factor receptor - گیرنده عامل فاکتور رشد یافته پلاکتEpithelial growth factor receptor - گیرنده فاکتور رشد اپیتلیال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
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چکیده انگلیسی
In epithelial tumors, the platelet-derived growth factor receptor B (PDGFRB) is mainly expressed by stromal cells of mesenchymal origin. Tumor cells may also acquire PDGFRB expression following epithelial-to-mesenchymal transition (EMT), which occurs during metastasis formation. Little is known about PDGFRB signaling in colorectal tumor cells. We studied the relationship between PDGFRB expression, EMT, and metastasis in human colorectal cancer (CRC) cohorts by analysis of gene expression profiles. PDGFRB expression in primary CRC was correlated with short disease-free and overall survival. PDGFRB was co-expressed with genes involved in platelet activation, transforming growth factor beta (TGFB) signaling, and EMT in three CRC cohorts. PDGFRB was expressed in mesenchymal-like tumor cell lines in vitro and stimulated invasion and liver metastasis formation in mice. Platelets, a major source of PDGF, preferentially bound to tumor cells in a non-activated state. Platelet activation caused robust PDGFRB tyrosine phosphorylation on tumor cells in vitro and in liver sinusoids in vivo. Platelets also release TGFB, which is a potent inducer of EMT. Inhibition of TGFB signaling in tumor cells caused partial reversion of the mesenchymal phenotype and strongly reduced PDGFRB expression and PDGF-stimulated tumor cell invasion. These results suggest that PDGFRB may contribute to the aggressive phenotype of colorectal tumors with mesenchymal properties, most likely downstream of platelet activation and TGFB signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neoplasia - Volume 15, Issue 2, February 2013, Pages 204-217, IN23-IN30
Journal: Neoplasia - Volume 15, Issue 2, February 2013, Pages 204-217, IN23-IN30
نویسندگان
Ernst J.A. Steller, Danielle A. Raats, Jan Koster, Bert Rutten, Klaas M. Govaert, Benjamin L. Emmink, Nikol Snoeren, Sander R. van Hooff, Frank C.P. Holstege, Coen Maas, Rinkes Inne H.M. Borel, Onno Kranenburg,