کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8297748 | 1536778 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ephrin-A1 expression induced by S100A8 is mediated by the toll-like receptor 4
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
TGFTLR4LLCMD-2S100A8SAA3serum amyloid A3Eph - افephrin - اهرینtransforming growth factor - تبدیل فاکتور رشدVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)Metastasis - متاستاز myeloid differentiation protein 2 - پروتئین تمایز میلوئیدی 2Lewis lung carcinoma - کارسینوم ریه لوئیس
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Ephrin-A1 expression induced by S100A8 is mediated by the toll-like receptor 4 Ephrin-A1 expression induced by S100A8 is mediated by the toll-like receptor 4](/preview/png/8297748.png)
چکیده انگلیسی
The deregulation of Eph/ephrin protein expression has been shown to lead to tumor development and progression. Both mRNA and protein expression analyses using clinical samples have demonstrated that ephrin-A1 is over-expressed in various cancers and positively correlates with a poor prognosis for cancer patients. The prognosis of cancer patients depends on metastasis to distant organs. We previously demonstrated that ADAM12 metalloproteinase cleaved ephrin-A1 and ADAM12-cleaved ephrin-A1 enhanced vascular permeability by degrading VE-cadherin and the EphA2 receptor at the plasma membrane. An increase of soluble ephrin-A1 levels in the serum facilitated tumor cell recruitment to the lungs, which resulted in lung metastasis. We also found that ephrin-A1 was overexpressed in 3LL tumors, a highly metastatic tumor, in mice and TNFα, an authentic positive regulator of ephrin-A1, was not elevated in the tumors, whereas S100A8 was. Moreover, S100A8 induced ephrin-A1 expression mediated by the toll-like receptor 4 (TLR4). S100A8 is known to be an endogenous ligand for TLR4 and its expression was shown to be increased in the lungs at the premetastatic phase. Thus, S100A8 and ephrin-A1 contribute to lung metastasis. Therefore, elucidating the regulation mechanism of ephrin-A1 overexpression is of importance and may lead to the development of therapeutic drugs against tumor growth and metastasis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 440, Issue 4, 1 November 2013, Pages 623-629
Journal: Biochemical and Biophysical Research Communications - Volume 440, Issue 4, 1 November 2013, Pages 623-629
نویسندگان
Katsuaki Ieguchi, Tsutomu Omori, Akiko Komatsu, Takeshi Tomita, Atsuko Deguchi, Yoshiro Maru,