التفاصيل البيبلوغرافية
| العنوان: |
Smad3 regulates E-cadherin via miRNA-200 pathway. |
| المؤلفون: |
Ahn, S-M1, Cha, J-Y2, Kim, J2, Kim, D2, Trang, H T H2, Kim, Y-M2, Cho, Y-H2, Park, D3, Hong, S2 |
| المصدر: |
Oncogene. 6/21/2012, Vol. 31 Issue 25, p3051-3059. 9p. |
| مصطلحات موضوعية: |
*SMAD proteins, *CADHERINS, *MICRORNA, *LUCIFERASES, *TRANSCRIPTION factors, *CANCER cell growth regulation, *GENETIC repressors |
| مستخلص: |
To identify potential microRNA (miRNA) links between Smad3, a mediator of TGF-β (transforming growth factor-β) signaling, and E-cadherin, we characterized the miRNA profiles of two gastric cancer cell lines: SNU484-LPCX, which does not express Smad3, and SNU484-Smad3, in which Smad3 is overexpressed. We found that among differentially expressed miRNAs, miR-200 family members are overexpressed in SNU484-Smad3 cells. Subsequent studies, including analysis of the effects of silencing Smad3 in SNU484-Smad3 cells and a luciferase reporter assay, revealed that Smad3 directly binds to a Smad-binding element located in the promoter region of miR-200b/a, where it functions as a transcriptional activator. TGF-β did not affect the regulatory role of Smad3 in transcription of miR-200 and expression of epithelial-mesenchymal transition markers. We conclude that Smad3 regulates, at the transcriptional level, miR-200 family members, which themselves regulate ZEB1 and ZEB2, known transcriptional repressors of E-cadherin, at the posttranscriptional level in a TGF-β-independent manner. This represents a novel link between Smad3 and posttranscriptional regulation by miRNAs in epithelial-mesenchymal transition in gastric cancer cells. [ABSTRACT FROM AUTHOR] |
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