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2017 ; 117
(2
): 233-244
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MicroRNA-199b-5p attenuates TGF-?1-induced epithelial-mesenchymal transition in
hepatocellular carcinoma
#MMPMID28588321
Zhou SJ
; Liu FY
; Zhang AH
; Liang HF
; Wang Y
; Ma R
; Jiang YH
; Sun NF
Br J Cancer
2017[Jul]; 117
(2
): 233-244
PMID28588321
show ga
BACKGROUND: Accumulating evidence indicates that N-cadherin is a cell adhesion
molecule that has critical roles in tumour progression. However, the role of
N-cadherin in hepatocellular carcinoma (HCC) remains controversial. METHODS: This
study aims to investigate the expression status of N-cadherin and its molecular
mechanisms in HCC. RESULTS: The expression of N-cadherin was markedly
overexpressed in HCC tissues and cell lines. We identified that miR-199b-5p binds
to the 3'-UTR of N-cadherin mRNA, thus decreasing N-cadherin expression in HCC
cells. We also found the downregulation of miR-199b-5p in HCC specimens, which
was inversely correlated with N-cadherin upregulation, predicted poor clinical
outcomes in HCC patients. Next, we determined that miR-199b-5p overexpression
promoted cell aggregation, suppressed cell migration and invasion in HCC cells,
and inhibited xenografts tumour metastasis in nude mice. Moreover, we
demonstrated that miR-199b-5p attenuated TGF-?1 induced epithelial-mesenchymal
transition (EMT) -associated traits, while its effects could be partially
reversed by N-cadherin restoration. Finally, we examined that N-cadherin
downregulation or miR-199b-5p overexpression suppressed TGF-?1-induced Akt
phosphorylation, and inhibition of PI3K/Akt pathway blocked TGF-?1-induced
N-cadherin overexpression in HCC cells. CONCLUSIONS: Our data demonstrate that
N-Cadherin was markedly overexpressed and miR-199b-5p was significantly
downregulated in HCC. MiR-199b-5p exerts inhibitory effects on EMT, and directly
targets N-cadherin in HCC, supporting the potential utility of miR-199b-5p as a
promising strategy to treat HCC. Also, a positive regulatory loop exists between
N-cadherin and Akt signalling represents a novel mechanism of TGF-?1-mediated EMT
in HCC cells.
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