Abstract |
MicroRNA-93, derived from a paralog (miR-106b-25) of the miR-17-92 cluster, is involved in the tumorigenesis and progression of many cancers such as breast, colorectal, hepatocellular, lung, ovarian, and pancreatic cancer. However, the role of miR-93 in endometrial carcinoma and the potential molecular mechanisms involved remain unknown. Our results showed that miR-93 was overexpressed in endometrial carcinoma tissues than normal endometrial tissues. The endometrial carcinoma cell lines HEC-1B and Ishikawa were transfected with miR-93-5P, after which cell migration and invasion ability and the expression of relevant molecules were detected. MiR-93 overexpression promoted cell migration and invasion, and downregulated E-cadherin expression while increasing N-cadherin expression. Dual- luciferase reporter assay showed that miR-93 may directly bind to the 3' untranslated region of forkhead box A1 (FOXA1); furthermore, miR-93 overexpression downregulated FOXA1 expression while miR-93 inhibitor transfection upregulated FOXA1 expression at both mRNA and protein level. In addition, transfection with the most effective FOXA1 small interfering RNA promoted both endometrial cancer cell migration and invasion, and downregulated E-cadherin expression while upregulating N-cadherin expression. Therefore, we suggest that miR-93 may promote the process of epithelial-mesenchymal transition in endometrial carcinoma cells by targeting FOXA1.
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Authors | Shuo Chen, Xi Chen, Kai-Xuan Sun, Yin-Ling Xiu, Bo-Liang Liu, Miao-Xiao Feng, Xiu-Bo Sang, Yang Zhao |
Journal | PloS one
(PLoS One)
Vol. 11
Issue 11
Pg. e0165776
( 2016)
ISSN: 1932-6203 [Electronic] United States |
PMID | 27829043
(Publication Type: Journal Article)
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Chemical References |
- 3' Untranslated Regions
- Antigens, CD
- CDH1 protein, human
- CDH2 protein, human
- Cadherins
- FOXA1 protein, human
- Hepatocyte Nuclear Factor 3-alpha
- MIRN93 microRNA, human
- MicroRNAs
- RNA, Small Interfering
- Luciferases
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Topics |
- 3' Untranslated Regions
- Antigens, CD
(genetics, metabolism)
- Binding Sites
- Cadherins
(genetics, metabolism)
- Cell Line, Tumor
- Cell Movement
- Cell Transformation, Neoplastic
(genetics, metabolism, pathology)
- Endometrial Neoplasms
(genetics, metabolism, pathology)
- Endometrium
(metabolism, pathology)
- Epithelial-Mesenchymal Transition
(genetics)
- Female
- Gene Expression Regulation, Neoplastic
- Genes, Reporter
- HEK293 Cells
- Hepatocyte Nuclear Factor 3-alpha
(antagonists & inhibitors, genetics, metabolism)
- Humans
- Luciferases
(genetics, metabolism)
- MicroRNAs
(genetics, metabolism)
- RNA, Small Interfering
(genetics, metabolism)
- Signal Transduction
- Transfection
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