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MiR‐194‐5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk

Authors :
Yi Zhang
Xiang Qing Li
Hong Liu
Yan Qu
Cui Liu
Shi‐Ying Ren
Hong Ma
Source :
Kaohsiung Journal of Medical Sciences, Vol 36, Iss 4, Pp 265-273 (2020)
Publication Year :
2020
Publisher :
Wiley, 2020.

Abstract

Wilms tumor (WT) is the most common solid childhood tumors all over the world. MicroRNAs (miRs) contribute to tumorigenesis of various cancers through targeting gene. The present study investigated the vital role of miR‐194‐5p and its underlying mechanism in the progression of WT. Immunohistochemistry and quantitative real‐time polymerase chain reaction (qRT‐PCR) assay indicated downregulation of miR194‐5p and upregulation of Crk, in WT tissues compared to adjacent normal tissues. Transfection with miR‐194‐5p mimics into nephroblastoma cells showed a significant decline in cell migration and invasion, which was detected by Transwell assay. Luciferase assay confirmed that Crk was a direct target gene of miR‐194‐5p. More important, the mesenchymal to epithelial transition (EMT) biomarkers containing E‐cadherin, N‐cadherin and Zeb1 were examined by Western blot, and revealed that miR‐194‐5p mimics decreased the levels of N‐cadherin and Zeb1 but increased E‐cadherin, which suggested that miR‐194‐5p inhibited EMT. Crk knockdown could reverse the increased nephroblastoma cell invasion, migration and EMT caused by miR‐194‐5p inhibitor. Interestingly, qRT‐PCR and Western blot analysis showed that overexpression of miR‐194‐5p deactivated HGF/c‐Met/Scr signaling pathway via targeting Crk. In conclusion, miR‐194‐5p inhibited nephroblastoma cell metastasis and EMT in the progression of WT by targeting Crk. Thus, miR‐194‐5p might be a potential target in WT particularly for the prevention of metastasis and EMT.

Details

ISSN :
24108650 and 1607551X
Volume :
36
Database :
OpenAIRE
Journal :
The Kaohsiung Journal of Medical Sciences
Accession number :
edsair.doi.dedup.....bfd3445d4e027ec87b5fbd582981963c
Full Text :
https://doi.org/10.1002/kjm2.12180