کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5586783 | 1568720 | 2017 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Interleukin-11-driven gastric tumourigenesis is independent of trans-signalling
ترجمه فارسی عنوان
تومورهای سرطانی ناشی از اینترلوکین 11 مستقل از انتقال سیگنال است
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کلمات کلیدی
STAT3ELANEIL-11TCGAgp130ADAM17SHPERKTNFαEGFRPI3KmTORJanus kinase - کیناز جانوس MAPK - MAPKADAM - آدامSTAT - آمارThe cancer genome atlas - اوتومتر ژنوم سرطانinterleukin-11 - اینترلوکین -11a disintegrin and metalloprotease - تخریب و متالوپروتئازtumour necrosis factor alpha - تومور نکروز عامل آلفاGastric cancer - سرطان معدهphosphoinositide 3-kinase - فسفینوزیتید 3-کینازSignal transducer and activator of transcription - مبدل سیگنال و فعال کننده رونویسیMechanistic target of rapamycin - هدف مکانیکی رپامایسینmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenproteinase 3 - پروتئیناز 3JAK - چگونهextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیglycoprotein 130 - گلیکوپروتئین 130Epidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
چکیده انگلیسی
Deregulated gp130-dependent STAT3 signalling by the pleiotropic cytokine interleukin (IL)-11 has been implicated in the pathogenesis of gastric cancer (GC), the third most common cancer worldwide. While the IL-11-gp130-STAT3 signalling axis has traditionally been thought to exclusively use the membrane-bound IL-11 receptor (mIL-11R), recent evidence suggests that mIL-11R can be proteolytically cleaved to generate a soluble form (sIL-11R) which can elicit trans-signalling. Since the role of IL-11 trans-signalling in disease pathogenesis is unknown, here we have employed the IL-11-driven gp130F/F spontaneous model of GC to determine whether IL-11 trans-signalling promotes gastric tumourigenesis. sIL-11R protein was detectable in gastric tissue from GC patients, and sIL-11R levels were elevated in tumours of gp130F/F mice compared to matched non-tumours. Among candidate proteases associated with the generation of sIL-11R, ADAM10 and the related metalloprotease ADAM17 were significantly upregulated in tumours of both gp130F/F mice and GC patients compared to matched non-tumour tissues. The genetic blockade of IL-11 trans-signalling in gp130F/F mice upon the transgenic over-expression of the trans-signalling antagonist, sgp130Fc, failed to suppress gastric inflammation and associated tumour growth, and also had no effect on reducing hyper-activated STAT3 levels. Furthermore, a non-essential role for ADAM17 in IL-11-driven gastric tumourigenesis was supported by the observation that the tumour burden was unaffected in gp130F/F:Adam17ex/ex mice in which ADAM17 expression levels have been substantially reduced. Collectively, these findings suggest that classic signalling rather than trans-signalling is the mode by which IL-11 promotes gastric tumourigenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 92, April 2017, Pages 118-123
Journal: Cytokine - Volume 92, April 2017, Pages 118-123
نویسندگان
Jesse J. Balic, Christoph Garbers, Stefan Rose-John, Liang Yu, Brendan J. Jenkins,