کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
575933 | 1453061 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Proteomic analysis of cell proliferation in a human hepatic cell line (HL-7702) induced by perfluorooctane sulfonate using iTRAQ
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کلمات کلیدی
myelocytomatosis oncogenemyelin transcription factor 1PFOSMYCITRAQWee13-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromideCDKs - CDK هاMTT - MTTcheckpoint kinase - بازرسی کینازisobaric tags for relative and absolute quantitation - برچسب های ایزوباریوم برای مقدار نسبی و مطلقCell proliferation - تکثیر سلولیCyclins - سیکلین هاcyclin-dependent kinase inhibitor 1A - مهار کننده 1A کیناز وابسته به کینازMyt1 - میت 1Chk - چاکCell cycle - چرخه سلولیcyclin-dependent kinases - کیناز وابسته به سیکلین
موضوعات مرتبط
مهندسی و علوم پایه
مهندسی شیمی
بهداشت و امنیت شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Perfluorooctane sulfonate (PFOS) is a commonly used and widely distributed perfluorinated compound proven to cause adverse health outcomes. However, how PFOS affects liver cell proliferation is not well understood. In this experiment, we exposed a human liver cell line (HL-7702) to 50 μM PFOS for 48 h and 96 h. We identified 52 differentially expressed proteins using a quantitative proteomic approach. Among them, 27 were associated with cell proliferation, including hepatoma-derived growth factor (Hdgf) and proliferation biomarkers Mk167 (Ki67) and Top2α. Results from MTT, cell counting, and cell cycle analysis showed low-dose PFOS (<200 μM) stimulated HL-7702 cell viability at 48 h and 96 h, reduced the G0/G1 percentage, and increased the S + G2/M percentage. Moreover, levels of Cyclin D1, Cyclin E2, Cyclin A2, Cyclin B1 and their partner Cdks were elevated, and the expression of regulating proteins like c-Myc, p53, p21 waf/cip1 and Myt1, as well as the phosphorylation levels of p-Wee1(S642), p-Chk1(S345) and p-Chk2(T68), were disturbed. We hypothesized that low-dose PFOS stimulated HL-7702 proliferation by driving cells into G1 through elevating cyclins/cdks expression, and by promoting cell cycle progression through altering other regulating proteins. This research will shed light on the mechanisms behind PFOS-mediated human hepatotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Hazardous Materials - Volume 299, 15 December 2015, Pages 361-370
Journal: Journal of Hazardous Materials - Volume 299, 15 December 2015, Pages 361-370
نویسندگان
Ruina Cui, Hongxia Zhang, Xuejiang Guo, Qianqian Cui, Jianshe Wang, Jiayin Dai,