کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10754817 | 1050362 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-497 inhibition of ovarian cancer cell migration and invasion through targeting of SMAD specific E3 ubiquitin protein ligase 1
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Ovarian cancer is the leading cause of death from gynecological malignancies worldwide. Understanding the molecular mechanism underlying ovarian cancer progression facilitates the development of promising strategy for ovarian cancer therapy. Previously, we observed frequent down-regulation of miR-497 expression in ovarian cancer tissues. In this study, we investigated the role of miR-497 in ovarian cancer metastasis. We found that endogenous miR-497 expression was down-regulated in the more aggressive ovarian cancer cell lines compared with the less aggressive cells. Exogenous expression of miR-497 suppressed ovarian cancer cell migration and invasion, whereas reduction of endogenous miR-497 expression induced tumor cell migration and invasion. Mechanistic investigations confirmed pro-metastatic factor SMURF1 as a direct target of miR-497 through which miR-497 ablated tumor cell migration and invasion. Further studies revealed that lower levels of miR-497 expression were associated with shorter overall survival as well as increased SMURF1 expression in ovarian cancer patients. Our results indicate that down-regulation of miR-497 in ovarian cancer may facilitate tumor metastasis. Restoration of miR-497 expression may be a promising strategy for ovarian cancer therapy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 449, Issue 4, 11 July 2014, Pages 432-437
Journal: Biochemical and Biophysical Research Communications - Volume 449, Issue 4, 11 July 2014, Pages 432-437
نویسندگان
Wei Wang, Fang Ren, Qinghua Wu, Dazhi Jiang, Hongjun Li, Zheng Peng, Jinglu Wang, Huirong Shi,