کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10915631 | 1090095 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Persistent STAT3 Activation in Colon Cancer Is Associated with Enhanced Cell Proliferation and Tumor Growth
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کلمات کلیدی
STAT3XenograftEMSAJanus kinase - کیناز جانوس Electrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزSTAT - آمارinterleukin - اینترلوکینCell proliferation - تکثیر سلولیColorectal cancer - سرطان روده بزرگcolorectal carcinoma - سرطان روده بزرگ و مقعدSignal transducer and activator of transcription - مبدل سیگنال و فعال کننده رونویسیJAK - چگونهCRC - کد افزونگی دورهای
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Colorectal carcinoma (CRC) is a major cause of morbidity and mortality in Western countries. It has so far been molecularly defined mainly by alterations of the Wnt pathway. We show here for the first time that aberrant activities of the signal transducer and activator of transcription STAT3 actively contribute to this malignancy and, thus, are a potential therapeutic target for CRC. Constitutive STAT3 activity was found to be abundant in dedifferentiated cancer cells and infiltrating lymphocytes of CRC samples, but not in non-neoplastic colon epithelium. Cell lines derived from malignant colorectal tumors lost persistent STAT3 activity in culture. However, implantation of colon carcinoma cells into nude mice resulted in restoration of STAT3 activity, suggesting a role of an extracellular stimulus within the tumor microenvironment as a trigger for STAT activation. STAT3 activity in CRC cells triggered through interleukin-6 or through a constitutively active STAT3 mutant promoted cancer cell multiplication, whereas STAT3 inhibition through a dominant-negative variant impaired IL-6-driven proliferation. Blockade of STAT3 activation in CRCderived xenograft tumors slowed down their development, arguing for a contribution of STAT3 to colorectal tumor growth.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neoplasia - Volume 7, Issue 6, June 2005, Pages 545-555
Journal: Neoplasia - Volume 7, Issue 6, June 2005, Pages 545-555
نویسندگان
Florian M. Corvinus, Carina Orth, Richard Moriggl, Svetlana A. Tsareva, Stefan Wagner, Edith B. Pfitzner, Daniela Baus, Roland Kaufman, Lukas A. Huber, Kurt Zatloukal, Hartmut Beug, Peter Ãhlschläger, Alexander Schütz, Karl-Jürgen Halbhuber,