کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2597380 | 1562409 | 2008 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Repression of Ah receptor and induction of transforming growth factor-β genes in DEN-induced mouse liver tumors
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کلمات کلیدی
PAI-1TGF-βXAP2ALDH3A1XRENQO1DREARNTbHLHDenAIPTCDDHSP90CDKAHR2,3,7,8-Tetrachlorodibenzo-p-dioxin - 2،3،7،8-تترا کلریدیبنزوپتوفان دیوکسینHCC - HCCAh receptor - آه گیرندهaryl hydrocarbon receptor nuclear translocator - اتمسفر هسته ای گیرنده آرویل کربنtransforming growth factor-beta - تبدیل فاکتور رشد بتاdiethylnitrosamine - دیاتیلنیتروستامینretinoblastoma - رتینوبلاستوما، تومور شبکیهAHRE - سالxenobiotic response element - عنصر واکنش زنجبیلdioxin response element - عنصر پاسخ دیوکسینAcute lymphoblastic leukemia - لوسمی لنفوبلاستیک حادPAS - نهALL - همهHeat shock protein 90 - پروتئین شوک حرارت 90plasminogen activator inhibitor type-1 - پلاسمینوژن فعال کننده مهار کننده نوع 1Tumor Suppressor Genes - ژن های سوپرسور تومورHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)cyclin-dependent kinase - کییناز وابسته به سیکلینaryl hydrocarbon receptor - گیرنده آرویل هیدروکربن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
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چکیده انگلیسی
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the biologic and toxic effects of its xenobiotic ligands. In recent years it has become evident that in the absence of ligand the AHR promotes cell cycle progression and that its activation by high-affinity ligands results in interactions with the retinoblastoma protein (RB) that lead to perturbation of the cell cycle, G0/G1 arrest, diminished capacity for DNA replication and inhibition of cell proliferation. Hence, the AHR has diametrically opposed pro-proliferative and anti-proliferative functions that have yet to be reconciled at the molecular level. Work from our own and from other laboratories suggests that the AHR may function as a tumor suppressor gene that becomes silenced in the process of tumor formation. To develop preliminary support for a more thorough examination of this hypothesis we characterized the expression levels of various tumor suppressor genes, transforming growth factor-β (Tgfb) genes and the Ahr gene in liver tumor samples from mice with a liver-specific RB ablation and their wild-type littermates. In tumors arising in RB-positive livers, Cdkn2d and Tgfb1 were repressed and Cdkn2c, Tgfb2, Tgfb3 and Pai1 were induced, whereas in RB-negative tumors, only Cdkn2c and Tgfb3 were induced. Ahr was significantly repressed in tumors from both sets of mice, supporting the concept that Ahr silencing may be associated with cancer progression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 246, Issues 2â3, 18 April 2008, Pages 242-247
Journal: Toxicology - Volume 246, Issues 2â3, 18 April 2008, Pages 242-247
نویسندگان
Li Peng, Christopher N. Mayhew, Michael Schnekenburger, Erik S. Knudsen, Alvaro Puga,