کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5649843 | 1407134 | 2017 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
An Interaction between Arsenic-Induced Epigenetic Modification and Inflammatory Promotion in a Skin Equivalent during Arsenic Carcinogenesis
ترجمه فارسی عنوان
تعامل بین اصلاح اپی ژنتیکی ناشی از آرسنیک و ارتقاء التهاب در یک معادل پوستی در حین سرطان زایی آرسنیک
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کلمات کلیدی
PBMCH3K9TGF-βtransforming growth factor-beta - تبدیل فاکتور رشد بتاtumor necrosis factor-alpha - تومور نکروز عامل آلفاPeripheral blood mononuclear cell - سلول تک هسته ای خون محیطیcytokeratin - سیتوکراتینTNF-α - فاکتور نکروز توموری آلفاFibroblast - فیبروبلاستSkin equivalent - معادل پوستKeratinocyte - کراتینوسیت
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
چکیده انگلیسی
Animal studies have shown that chemical carcinogenesis consists of a three-stage process: initiation, promotion, and progression. However, because of the lack of a suitable tissue model, the molecular mechanisms of cell-cell interactions involved in those processes remain unclear. We have established a human intraepidermal carcinoma skin equivalent with organotypic culture-consisting of keratinocytes, fibroblasts, and peripheral blood mononuclear cells - induced by arsenic treatment. This SE shows the pathognomonic characteristics of arsenic-induced Bowen's disease, including acanthosis, dysplasia, and dyskeratosis. Using this SE model, we showed that arsenic initiated SUV39H2-mediated epigenetic modification of E2F1, which induced centrosome amplification in keratinocytes in 2 days; this, however, led to caspase-8-mediated apoptosis in 10 days. In parallel, arsenic stimulated tumor necrosis factor-α release mainly from peripheral blood mononuclear cells. Tumor necrosis factor-α triggered anti-apoptotic signals via FLIP-associated caspase-8 inactivation in arsenic-treated keratinocytes, which in turn contributed to cell survival and aneuploidy. The interaction between arsenic-induced epigenetic modification and inflammatory promotion resulted in the development of the pathognomonic features of arsenic-induced Bowen's disease in this model.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 137, Issue 1, January 2017, Pages 187-196
Journal: Journal of Investigative Dermatology - Volume 137, Issue 1, January 2017, Pages 187-196
نویسندگان
Wei-Ting Liao, Jian-He Lu, Chih-Hung Lee, Cheng-Che E. Lan, Jan-Gowth Chang, Chee-Yin Chai, Hsin-Su Yu,