کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10914740 | 1088810 | 2014 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Collective migration of cancer-associated fibroblasts is enhanced by overexpression of tight junction-associated proteins claudin-11 and occludin
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
ICCMWLCALDMEHPOCLNIGPECMTGF-βPLAUCAFlamb1mono-(2-ethylhexyl) phthalate - mono (2-ethylhexyl) phthalateImmunocytochemistry - ایمونوسیتوشیمیIHC - ایمونوهیستوشیمیImmunohistochemistry - ایمونوهیستوشیمیstable isotope labeling with amino acids in cell culture - برچسب زدن ایزوتوپ پایدار با اسیدهای آمینه در کشت سلولیtransforming growth factor-beta - تبدیل فاکتور رشد بتاEMT - تکنسین فوریتهای پزشکیconditioned media - رسانه های متعلق بهColorectal cancer - سرطان روده بزرگSILAC - سیلکOccludin - عذابurokinase-type plasminogen activator - فعال کننده پلاسمینوژن نوع urokinaseCancer-associated fibroblasts - فیبروبلاست های مرتبط با سرطانcancer-associated fibroblast - فیبروبلاست وابسته به سرطانExtracellular matrix - ماتریکس خارج سلولیMigration - مهاجرتCaldesmon - کالدسونگClaudin-11 - کلودین-11epithelial-to-mesenchymal transition - گذار اپیتلیال به مزانشیمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
It has been suggested that cancer-associated fibroblasts (CAFs) positioned at the desmoplastic areas of various types of cancer are capable of executing a migratory program, characterized by accelerated motility and collective configuration. Since CAFs are reprogrammed derivatives of normal progenitors, including quiescent fibroblasts, we hypothesized that such migratory program could be context-dependent, thus being regulated by specific paracrine signals from the adjacent cancer population. Using the traditional scratch assay setup, we showed that only specific colon cancer cell lines (i.e. HT29) were able to induce collective CAF migration. By performing quantitative proteomics (SILAC), we identified a 2.7-fold increase of claudin-11, a member of the tight junction apparatus, in CAFs that exerted such collectivity in their migratory pattern. Further proteomic investigations of cancer cell line secretomes revealed a specific signature, involving TGF-β, as potential mediator of this effect. Normal colonic fibroblasts stimulated with TGF-β exerted myofibroblastic differentiation, occludin (OCLN) and claudin-11 (CLDN11) overexpression and cohort formation. Subsequently, inhibition of TGF-β attenuated all the previous effects. Immunohistochemistry of the universal tight junction marker occludin in a cohort of 30 colorectal adenocarcinoma patients defined a CAF subpopulation expressing tight junctions. Overall, these data suggest that cancer cells may induce CLDN11 overexpression and subsequent collective migration of peritumoral CAFs via TGF-β secretion.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Oncology - Volume 8, Issue 2, March 2014, Pages 178-195
Journal: Molecular Oncology - Volume 8, Issue 2, March 2014, Pages 178-195
نویسندگان
George S. Karagiannis, David F. Schaeffer, Chan-Kyung J. Cho, Natasha Musrap, Punit Saraon, Ihor Batruch, Andrea Grin, Bojana Mitrovic, Richard Kirsch, Robert H. Riddell, Eleftherios P. Diamandis,