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| Content Provider | Springer Nature Link |
|---|---|
| Author | Zeng, Jun Wei, Min Shi, Rong Cai, Cuixia Liu, Xinrui Li, Taoping Ma, Wenli |
| Copyright Year | 2015 |
| Abstract | Epithelial–mesenchymal transition (EMT) is a vital process in epithelial cancer invasion and metastasis. The induction of EMT by Six1 has been described as a common mode of cancer progression, which could promote breast cancer migration and invasion. In the study, we found that miR-204-5p could suppress the migration and invasion of breast cancer cell lines. Since overexpression of Six1 promote EMT, we identified a mechanism by which miR-204-5p inhibited the EMT by downregulating the Six1, which was mediated by a conserved miR-204-5p seed-matching sequence in the 3′-UTR of Six1 mRNA. We also identified that upregulation of Six1 could downregulate miR-204-5p expression, affecting the migration and invasion of breast cancer cell lines. In conclusion, the frequent upregulation of Six1 and/or downregulation of miR-204-5p in breast cancer may shift the equilibrium of these reciprocal regulations and lock breast cancer cells in the mesenchymal state. |
| Starting Page | 2729 |
| Ending Page | 2735 |
| Page Count | 7 |
| File Format | |
| ISSN | 10104283 |
| Journal | Tumor Biology |
| Volume Number | 37 |
| Issue Number | 2 |
| e-ISSN | 14230380 |
| Language | English |
| Publisher | Springer Netherlands |
| Publisher Date | 2015-09-25 |
| Publisher Place | Dordrecht |
| Access Restriction | Subscribed |
| Subject Keyword | miR-204-5p Six1 EMT Breast cancer Cancer Research |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Cancer Research |
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