کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10904247 | 1086569 | 2013 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Norepinephrine inhibits the migratory activity of pancreatic cancer cells
ترجمه فارسی عنوان
نوراپی نفرین فعالیت مهاجرت سلول های سرطانی پانکراس را مهار می کند
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کلمات کلیدی
GPCRPIP2PDGFRPLCγEGFRIP3FITCG protein coupled receptor - G پروتئین همراه با پروتئینtransforming growth factor - تبدیل فاکتور رشدphospholipase Cγ - فسفولیپاز Cγfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتCell migration - مهاجرت سلولیnorepinephrine - نوراپی نفرینSignal transduction - هدایت سیگنالplatelet-derived growth factor receptor - گیرنده عامل فاکتور رشد یافته پلاکتEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمالbeta-adrenergic receptors - گیرنده های بتا آدرنرژیک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
چکیده انگلیسی
We have shown previously that norepinephrine induces migratory activity of tumour cells from breast, colon and prostate tissue via activation of beta-2 adrenergic receptors. Consequently, this effect can be inhibited pharmacologically by clinically established beta-blockers. Tumour cell migration is a prerequisite for metastasis formation, and accordingly we and others have shown that breast cancer patients, which take beta-blockers due to hypertension, have reduced metastasis formation and increased survival probability as compared to patients without hypertension or using other anti-hypertensive medication. Unlike the aforementioned tumour cells, pancreatic cancer cells show a reduced migratory activity upon norepinephrine treatment. By means of our three-dimensional, collagen-based cell migration assay, we have investigated the signal transduction pathways involved in this phenomenon. We have found that this conflicting effect of norepinephrine on pancreatic cancer cells is due to an imbalanced activation of the two pathways that usually mediate a pro-migratory effect of norepinephrine in other tumour cell types. Firstly, the inhibitory effect results from activation of a pathway which causes a strong increase of the secondary cell signalling molecule, cAMP. In addition, activation of phospholipase C gamma and the downstream protein kinase C alpha were shown to be already activated in pancreatic cancer cells and cannot be further activated by norepinephrine. We hypothesize that this constitutive activation of the phospholipase C gamma pathway is due to a cross-talk with receptor tyrosine kinase signalling, and this might also deliver an explanation for the unusual high spontaneous migratory activity of pancreatic cancer cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 319, Issue 12, 15 July 2013, Pages 1744-1758
Journal: Experimental Cell Research - Volume 319, Issue 12, 15 July 2013, Pages 1744-1758
نویسندگان
Anna-Maria Stock, Desmond G. Powe, Stephan A. Hahn, Gabriele Troost, Bernd Niggemann, Kurt S. Zänker, Frank Entschladen,