کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5918331 | 1163858 | 2008 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Non-small cell lung cancer cells produce a functional set of complement factor I and its soluble cofactors
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کلمات کلیدی
ADCCMCPCDCmembrane cofactor protein (CD46)DAFFHL-1PKCC4bpCCPCDCCTumor - تومورComplement factor H - تکمیل عامل HImmune system - دستگاه ایمنی یا سیستم ایمنیNSCLC - سرطان ریوی غیر سلول کوچکNon-small cell lung cancer - سرطان غیر سلول کوچک ریهCytotoxicity - سمیت سلولیAntibody-dependent cell cytotoxicity - سمیت سلولی وابسته به آنتی بادیcomplement-dependent cytotoxicity - سمیت سلولی وابسته به مکملComplement Factor I - فاکتور تکمیلی IComplement - متممMAC - مکC4b-binding protein - پروتئین C4b اتصالProtein S - پروتئین Scomplement control protein - پروتئین کنترل مکملProtein kinase C - پروتئین کیناز سیcomplement receptor 1 - گیرنده مکمل 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
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چکیده انگلیسی
The complement system is important for protection from invading pathogens, removal of waste products and guidance of the immune response. Furthermore, complement can be also targeted to cancer cells. However, membrane-bound inhibitors over-expressed by certain types of tumor cells restrict the cytotoxic activity of complement. Herein we report that non-small cell lung cancer (NSCLC) cells produce soluble complement inhibitors factor I (FI) and C4b-binding protein (C4BP). FI is a serine protease capable of degrading the activated complement components C3b and C4b, whilst C4BP acts as its cofactor. Furthermore, NSCLC cells express membrane-bound regulators and shed membrane cofactor protein (MCP), which shares cofactor function with C4BP. Secretion of FI from NSCLC cells was higher than previously reported for any non-hepatic source and FI produced by these cells could efficiently support cleavage of C3b and C4b. In vitro functional assays revealed that additional FI significantly decreased C3 deposition and complement-dependent lysis, particularly when cofactors were added. Our results demonstrate that soluble inhibitors produced by NSCLC cells may provide further protection from complement beyond the level ensured by membrane-bound inhibitors and, as such, contribute to the aggressive phenotype of these lung cancer cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 45, Issue 1, January 2008, Pages 169-179
Journal: Molecular Immunology - Volume 45, Issue 1, January 2008, Pages 169-179
نویسندگان
Marcin Okroj, Yi-Fan Hsu, Daniel Ajona, Ruben Pio, Anna M. Blom,