کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10749824 | 1050295 | 2015 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
miR-503 suppresses metastasis of hepatocellular carcinoma cell by targeting PRMT1
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Accumulating evidence indicates that microRNAs function as oncogenes or tumor suppressor genes in human cancer. MiR-503 is deregulated in various human cancers and has been associated with hepatocellular carcinoma (HCC) progression. However, the underlying mechanisms of miR-503 involvement in the development and progression of HCC remains poorly understood. In the present study, we report that miR-503 suppresses cell metastasis in HCC through targeting the protein arginine methyl transferase 1 (PRMT1) mRNA. Notably, we identiï¬ed that miR-503 was able to target 3â²-untranslated region (3â²-UTR) of PRMT1 mRNA by luciferase reporter gene assays. Then, we revealed that miR-503 was able to reduce the expression of PRMT1 at the levels of mRNA and protein using RT-PCR and Western blotting analysis. The expression levels of miR-503 were negatively related to those of PRMT1 mRNA in clinical HCC tissues. In terms of function, transwell and wound healing assays demonstrated that the miR-503 remarkably inhibited invasion and migration of HCC cells, which was reversed by overexpressed PRMT1. Furthermore, exogenous expression of miR-503 dramatically suppressed epithelial-mesenchymal transition (EMT) via PRMT1 in HCC cells. In conclusion, we denomstrated PRMT1 as a novel target gene of miR-503 and miR-503-mediated PRMT1 could also emerge as a potential important biomarker for HCC.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 464, Issue 4, 4 September 2015, Pages 982-987
Journal: Biochemical and Biophysical Research Communications - Volume 464, Issue 4, 4 September 2015, Pages 982-987
نویسندگان
Bingshou Li, Lin Liu, Xiaoming Li, Lingtong Wu,