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MiR-429 increases the metastatic capability of HCC via regulating classic Wnt pathway rather than epithelial-mesenchymal transition.

Abstract：

:Epigenetic modification of miR-429 can manipulate liver T-ICs via targeting the RBBP4/E2F1/Oct4 axis, which might be crucial for hepatocarcinogenesis. However, whether miR-429 plays a role in regulating metastasis of hepatocellular carcinoma is still unclear. Using quantitative methylation analysis and real-time PCR, we have identified the hypomethylated status and upregulation of miR-429 in portal vein metastasis samples in comparison with their matched primary tumor. The ectopic expression of miR-429 dramatically induced the expression of MMP2/7/9 and enhanced HCC migration and invasion in vitro and in vivo in an EMT-independent manner. Both bioinformatics and functional studies elucidated the direct regulation of miR-429 on the 3'UTR of the PTEN gene, which leads to the activation of PI3K/AKT signaling and the nuclear translocation of β-catenin, eventually. Conversely, the knockdown of miR-429 efficiently recovered the expression of PTEN and attenuated PI3K/AKT/β-catenin-mediated cell metastasis. Clinically, the higher expression of miR-429 and nucleus relocation of β-catenin were identified as the adverse prognosis factors for recurrence-free survival (RFS) and overall survival (OS). In summary, our results here defined miR-429 as a key inducer for HCC pathogenesis and metastasis with potential utility for tumor intervention.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Tang J,Li L,Huang W,Sui C,Yang Y,Lin X,Hou G,Chen X,Fu J,Yuan S,Li S,Wen W,Tang S,Cao D,Wu M,Chen L,Wang H

doi

10.1016/j.canlet.2015.04.023

subject

Has Abstract

pub_date

2015-08-01 00:00:00

pages

33-43

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(15)00291-8

journal_volume

364

pub_type

杂志文章

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