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Tumour Biol. 2016 Feb;37(2):2729-35. doi: 10.1007/s13277-015-4039-1. Epub 2015 Sep 25.

MiR-204-5p/Six1 feedback loop promotes epithelial-mesenchymal transition in breast cancer.

Author information

1
Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
2
Sleep Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China. ltpnet@126.com.
3
Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China. Wenlimat@126.com.

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.

KEYWORDS:

Breast cancer; EMT; Six1; miR-204-5p

PMID:
26408179
DOI:
10.1007/s13277-015-4039-1
[Indexed for MEDLINE]

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