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Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells.

Authors :
Wang, Jian
Zhao, Xiangzhai
Guo, Zhaojun
Ma, Xiaolin
Song, Yueqing
Guo, Ying
Source :
Archives of Gynecology & Obstetrics. Jun2017, Vol. 295 Issue 6, p1469-1475. 7p. 4 Graphs.
Publication Year :
2017

Abstract

<bold>Objective: </bold>To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells.<bold>Materials and Methods: </bold>NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by Western blot. The effects of NEAT1, HMGA1, miR-214-3p on the viability, migration and invasion of HEC-1A cells were accessed by WST-1 assay and transwell migration/invasion assay. The effect of miR-214-3p on Wnt signaling activity was tested by luciferase reporter assay.<bold>Results: </bold>NEAT1, HMGA1 and β-catenin were significantly upregulated in EC tissues, and miR-214-3p was significantly downregulated. NEAT1 promoted the growth, migration and invasion of HEC-1A cells, and mRNA level of Wnt/β-catenin downstream genes c-myc and MMP9. In addition, HMGA1 upregualted the protein and mRNA levels of Wnt/β-catenin downstream genes c-myc and MMP9, and could improve cell viability, and increase numbers of migration and invasion of HEC-1A cells. miR-214-3p overexpression inhibited the proliferation, migration and invasion of HEC-1A cells, while NEAT1 overexpression reversed these effects. miR-214-3p overexpression inhibited the activity of Wnt/β-catenin pathway, while NEAT1 overexpression reversed this effect. Then, si-HMGA1 reduced the activity of Wnt/β-catenin pathway. Moreover, we found NEAT1 and HMGA1 bound to miR-214-3p by luciferase reporter assay, and NEAT1 and HMGA1 expression were negatively correlated with miR-214-3p.<bold>Conclusion: </bold>NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/β-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
09320067
Volume :
295
Issue :
6
Database :
Academic Search Index
Journal :
Archives of Gynecology & Obstetrics
Publication Type :
Academic Journal
Accession number :
123023095
Full Text :
https://doi.org/10.1007/s00404-017-4365-1