کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9244065 | 1209899 | 2005 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Macrophage Migration Inhibitory Factor Promotes Intestinal Tumorigenesis
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کلمات کلیدی
NF-κBLppCMVDAPCTBSHPPFFPE - MEPenzyme-linked immunoassay - آزمایش ایمنی مرتبط با آنزیمrecombinant human - انسان نوترکیبEIA - اینMicrovessel density - تراکم MicrovesselTris-buffered saline - تریس بافر شورminimal essential medium - حداقل وسایل ضروریSmall intestine - روده کوچکColorectal cancer - سرطان روده بزرگplasma cell - سلول پلاسماMIF - شهرnuclear factor-κB - فاکتور هسته ای κBformalin-fixed, paraffin-embedded - فرمالین ثابت، پارافین تعبیه شده استMEM - مامانpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازoptical density - چگالی نوریCRC - کد افزونگی دورهای
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: The cytokine macrophage migration inhibitory factor (MIF) is expressed throughout the human gastrointestinal tract. Recently, protumorigenic activity of MIF has been described in several cancer models. Therefore, we investigated the expression and function of MIF during the early stages of intestinal tumorigenesis. Methods: MIF messenger RNA, protein, and tautomerase activity were measured in normal intestinal mucosa and adenomas from patients with sporadic colorectal adenomas and in the adenomatous polyposis coli (Apc)Min/+ mouse model of intestinal tumorigenesis. MIF function was investigated by using VACO-235 human colorectal adenoma cells in vitro and by testing the effect of genetic deletion of Mif on ApcMin/+ mouse intestinal tumorigenesis. Results: MIF expression and tautomerase activity were increased in human and ApcMin/+ mouse intestinal adenomas compared with adjacent normal mucosa. Up-regulation of MIF occurred mainly in epithelial cells (associated with an increasing grade of dysplasia), but also in stromal plasma cells. Exogenous MIF inhibited apoptosis and promoted anchorage-independent growth of VACO-235 cells (maximal at 100 ng/mL). Homozygous deletion of Mif was associated with a reduction in the number and size of ApcMin/+ mouse adenomas (P = .025 for the difference in large [>7-mm] tumors) and decreased angiogenesis (43% decrease in mean tumor microvessel density), but there was no alteration in epithelial cell apoptosis or proliferation. Conclusions: MIF expression is increased in sporadic human colorectal adenomas, and exogenous MIF drives tumorigenic behavior of epithelial cells in vitro. Mif also promotes intestinal tumorigenesis (predominantly via angiogenesis) in the ApcMin/+ mouse. Therefore, MIF is a potential colorectal cancer chemoprevention target.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 129, Issue 5, November 2005, Pages 1485-1503
Journal: Gastroenterology - Volume 129, Issue 5, November 2005, Pages 1485-1503
نویسندگان
Jonathan M. Wilson, P. Louise Coletta, Richard J. Cuthbert, Nigel Scott, Kenneth MacLennan, Gillian Hawcroft, Lin Leng, Jodi B. Lubetsky, Kai K. Jin, Elias Lolis, Francisco Medina, Jose A. Brieva, Richard Poulsom, Alexander F. Markham, Richard Bucala,