کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1938069 | 1050731 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The variation in Fas localization and the changes in Fas expression level upon stimulation with growth factors
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کلمات کلیدی
FCMTNFFas-LFASCLSMIGFPBSEGFinsulin-like growth factor I - انسولین مانند عامل رشد Iimmunoglobulin - ایمونوگلوبولینApoptosis - خزان یاختهایInternalization - داخلی سازیepidermal growth factor - عامل رشد اپیدرمیFas-ligand - فاس لیگندGrowth factor - فاکتور رشدVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)tumor necrosis factor - فاکتور نکروز تومورFlow cytometry - فلوسیتومتریConfocal laser scanning microscope - میکروسکوپ اسکن لیزر ConfocalAntibody - پادتَن یا آنتیبادی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Although Fas (APO-1/CD95) is well known as a death receptor, its stimulation occasionally fails to induce apoptosis in malignant cells. On the contrary, Fas is reported to advance the cell cycle in cancer cells. Therefore, we investigated roles of Fas in cell growth and apoptosis using human lung cancer cell lines. Fas was localized in the cytoplasm in exponentially growing cells, whereas only confluent cells expressed Fas on the cell membrane. A stimulation of confluent cells by either of EGF, IGF-I or VEGF induced once a decrease in Fas expression level and its sequential recovery. Fas expression levels in confluent cells were negatively correlated with cell doubling times (r = 0.757, p = 0.0088). Fas remained on the cell membrane of IgM-treated cells even after the growth factor stimulation, leading to apoptosis with abnormal mitosis, whereas the same stimulation induced Fas internalization in IgG1-treated cells. From these results, we suggest that Fas remaining on the cell membrane amplifies to induce apoptosis. Conversely, Fas internalization may enable cancer cells to escape from apoptosis. Our results suggest that growth factor may contribute to the resistance of cancer cells to Fas-mediated apoptosis in an autocrine or paracrine fashion.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 353, Issue 1, 2 February 2007, Pages 159-163
Journal: Biochemical and Biophysical Research Communications - Volume 353, Issue 1, 2 February 2007, Pages 159-163
نویسندگان
Kazuki Omoteyama, Shoichi Inoue,