MiR-204-5p/Six1 feedback loop promotes epithelial–mesenchymal transition in breast cancer
| Autor: | Taoping Li, Xin-rui Liu, Jun Zeng, Cuixia Cai, Rong Shi, Wen-Li Ma, Min Wei |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Oncology medicine.medical_specialty Epithelial-Mesenchymal Transition Down-Regulation Breast Neoplasms Biology Cell Line Metastasis 03 medical and health sciences 0302 clinical medicine Breast cancer Downregulation and upregulation Cell Movement Cell Line Tumor Internal medicine microRNA medicine Humans RNA Messenger Epithelial–mesenchymal transition 3' Untranslated Regions Homeodomain Proteins Mesenchymal stem cell HEK 293 cells Cancer General Medicine medicine.disease Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs HEK293 Cells 030104 developmental biology 030220 oncology & carcinogenesis MCF-7 Cells Cancer research Female |
| Zdroj: | Tumor Biology. 37:2729-2735 |
| ISSN: | 1423-0380 1010-4283 |
| DOI: | 10.1007/s13277-015-4039-1 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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