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)...
Saved in:
Published in | Journal of Cancer Vol. 11; no. 12; pp. 3424 - 3432 |
---|---|
Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Ivyspring International Publisher Pty Ltd
01.01.2020
Ivyspring International Publisher |
Subjects | |
Online Access | Get full text |
Cover
Loading…
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 |