کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2151932 | 1090033 | 2009 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CD44v6 Dependence of Premetastatic Niche Preparation by Exosomes
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کلمات کلیدی
BSp73ASMLBMCHAS3TSPCancer-Initiating CellCD44vCICLNCIFPRAECHyaluronic acid - اسید هیالورونیکThrombospondin - ترومبوزپوندینcomplement component 3 - جزء مکمل 3Bone marrow cell - سلول مغز استخوانlymph node cells - سلول های گره لنفاویConditioned medium - شرایط محیطیLung fibroblasts - فیبروبلاست های ریهFibronectin - فیبرونکتینwild type - نوع وحشیVitronectin - ویترونکتینColl - کلاCollagen - کلاژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
The metastasizing capacity of the rat pancreatic adenocarcinoma BSp73ASML (ASMLwt) is strikingly reduced by a knockdown of CD44v4-v7 (ASMLkd). We used this model to analyze the role of the CD44 variant isoform (CD44v) in (pre)metastatic niche formation. Intrafootpad injections of ASMLwt-, but not ASMLkd-conditioned medium (CM), strongly promote settlement of ASMLkd cells in lymph nodes and lung. Fractionation of CM revealed a contribution by a soluble matrix and exosomes, where the CD44v6-containing ASMLwt-soluble fraction can complement ASMLkd-exosomes, but not vice versa. This implies that exosomes are the final actors, are CD44v-independent, but require a soluble matrix, which depends on CD44v. Analyzing the composition revealed that only the ASMLwt-matrix contains c-Met and urokinase-type plasminogen activator receptor. In vitro, mostly ASMLwt-exosomes promote proliferation and induce gene expression in metastatic organ cells. However, in vivo corresponding changes in the (pre) metastatic organ are only observed when both, exosomes plus the soluble matrix, are provided. Thus, neither CD44v nor exosomes alone suffice for (pre)metastatic niche formation. Instead, CD44v suffices for assembling a soluble matrix, which allows exosomes, independent of their origin from poorly or highly metastatic cells, to modulate (pre) metastatic organ cells for tumor cell embedding and growth.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neoplasia - Volume 11, Issue 10, October 2009, Pages 1093-1105, IN13-IN17
Journal: Neoplasia - Volume 11, Issue 10, October 2009, Pages 1093-1105, IN13-IN17
نویسندگان
Thorsten Jung, Donatello Castellana, Pamela Klingbeil, Ines Cuesta Hernández, Mario Vitacolonna, David J. Orlicky, Steve R. Roffler, Pnina Brodt, Margot Zöller,