MiR-425 Promotes Migration and Invasion in Bladder Cancer by Targeting Dickkopf 3

Bladder cancer (BC) is a common malignancy with high morbidity and mortality. MicroRNAs (miRNAs) are critical post-transcriptional regulators in various cancers. This study aimed to investigate the effect of miR-425 on the migration and invasion of BC. The expression of miR-425 and Dickkopf 3 (DKK3)...

Full description

Saved in:
Bibliographic Details
Published inJournal of Cancer Vol. 11; no. 12; pp. 3424 - 3432
Main Authors Ning, Jin-Zhuo, Yu, Wei-Min, Cheng, Fan, Rao, Ting, Ruan, Yuan
Format Journal Article
LanguageEnglish
Published Australia Ivyspring International Publisher Pty Ltd 01.01.2020
Ivyspring International Publisher
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Bladder cancer (BC) is a common malignancy with high morbidity and mortality. MicroRNAs (miRNAs) are critical post-transcriptional regulators in various cancers. This study aimed to investigate the effect of miR-425 on the migration and invasion of BC. The expression of miR-425 and Dickkopf 3 (DKK3) was examined in clinical BC specimens. T24 and 5637 BC cell lines were employed and transfected with miR-425 inhibitors. The correlation between miR-425 and DKK3 was determined by a luciferase reporter assay. Cell migration and invasion capacity were measured by wound healing and Transwell assays. The expression levels of DKK3, E-cadherin, N-cadherin and vimentin were analysed by Western blotting and qRT-PCR. miR-425 was negatively correlated with the expression of DKK3 in clinical BC specimens. Further studies identified DKK-3 as a direct target of miR-425. Moreover, knockdown of miR-425 promoted the expression of DKK3 and suppressed cell migration and invasion capacity. miR-425 silencing increased E-cadherin levels but decreased vimentin and N-cadherin protein levels in T24 and 5637 cells. Our study indicated that miR-425 promoted the migration and invasion of BC via targeting DKK3.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Competing Interests: The authors have declared that no competing interest exists.
Contributed equally
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.40233