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Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
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MicroRNA-194 inhibits epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1
This item is licensed under:Creative Commons Attribution 2.0 Generic
| Title: | MicroRNA-194 inhibits epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1 |
| Authors: | Dong, Peixin Browse this author | | Kaneuchi, Masanori Browse this author | | Watari, Hidemichi Browse this author | | Hamada, Junichi Browse this author | | Sudo, Satoko Browse this author | | Ju, Jingfang Browse this author | | Sakuragi, Noriaki Browse this author →KAKEN DB |
| Issue Date: | 18-Aug-2011 |
| Publisher: | BioMed Central |
| Journal Title: | Molecular Cancer |
| Volume: | 10 |
| Start Page: | 99 |
| Publisher DOI: | 10.1186/1476-4598-10-99 |
| Abstract: | Background: Epithelial-mesenchymal transition (EMT) is the key process driving cancer metastasis. Oncogene/self renewal factor BMI-1 has been shown to induce EMT in cancer cells. Recent studies have implied that noncoding microRNAs (miRNAs) act as crucial modulators for EMT. The aims of this study was to determine the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of miRNA in controlling BMI-1 expression. Methods and results: We evaluated the expression of BMI-1 gene in a panel of EC cell lines, and detected a strong association with invasive capability. Stable silencing of BMI-1 in invasive mesenchymal-type EC cells up-regulated the epithelial marker E-cadherin, down-regulated mesenchymal marker Vimentin, and significantly reduced cell invasion in vitro. Furthermore, we discovered that the expression of BMI-1 was suppressed by miR-194 via direct binding to the BMI-1 3'-untranslated region 3'-UTR). Ectopic expression of miR-194 in EC cells induced a mesenchymal to epithelial transition (MET) by restoring E-cadherin, reducing Vimentin expression, and inhibiting cell invasion in vitro. Moreover, BMI-1 knockdown inhibited in vitro EC cell proliferation and clone growth, correlated with either increased p16 expression or decreased expression of stem cell and chemoresistance markers (SOX-2, KLF4 and MRP-1). Conclusion: These findings demonstrate the novel mechanism for BMI-1 in contributing to EC cell invasion and that repression of BMI-1 by miR-194 could have a therapeutic potential to suppress EC metastasis. |
| Rights: | http://creativecommons.org/licenses/by/2.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/47213 |
| Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 櫻木 範明
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