title: MiR-204-5p/Six1 feedback loop promotes epithelial-mesenchymal transition in breast cancer.
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.
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
authors.forename: Jun
authors.initials: J
authors.lastname: Zeng
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
authors.forename: Min
authors.initials: M
authors.lastname: Wei
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
authors.forename: Rong
authors.initials: R
authors.lastname: Shi
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
authors.forename: Cuixia
authors.initials: C
authors.lastname: Cai
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China.
authors.forename: Xinrui
authors.initials: X
authors.lastname: Liu
authors.affiliation: Sleep Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China. ltpnet@126.com.
authors.forename: Taoping
authors.initials: T
authors.lastname: Li
authors.affiliation: Institute of Genetic Engineering, Southern Medical University, No.1838, Baiyun Road North, Guangzhou, People's Republic of China. Wenlimat@126.com.
authors.forename: Wenli
authors.initials: W
authors.lastname: Ma
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology*; D002460:Cell Line; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D015536:Down-Regulation / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D057809:HEK293 Cells; D018398:Homeodomain Proteins / Q000235:genetics*; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics
chemical_list: D020413:3' Untranslated Regions; D018398:Homeodomain Proteins; C549404:MIRN204 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; C099236:SIX1 protein, human
keywords: Breast cancer; EMT; Six1; miR-204-5p