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Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and
promotes epithelial-mesenchymal transition
#MMPMID27073719
Wang SH
; Wu XC
; Zhang MD
; Weng MZ
; Zhou D
; Quan ZW
Am J Cancer Res
2016[]; 6
(1
): 15-26
PMID27073719
show ga
The imprinted oncofetal long non-coding RNA H19 has been reported to be involved
in many kinds of human cancers. However, whether lncRNA H19 implicate in
oncogenesis and cancer progression in gallbladder cancer remain largely unknown.
In the present study, compared with adjacent normal tissues, the level of H19 was
significantly upregulated in gallbladder cancer tissues and was positively
associated with lymphatic metastasis and tumor size. The overall survival is
shorter in those who had higher H19 expression among GBC patients. In vitro, both
TGF-?1 and IL-6 treatment induced upregulation of H19, downregulated the protein
level of E-cadherin while increased Vimentin, indicating an
epithelial-mesenchymal transition (EMT) phenotype in GBC. The overexpression of
H19 in GBC cells enhanced tumor invasion and promoted EMT by upregulated
transcription factor Twist1. On the contrary, Loss of function studies indicated
that H19 interference in GBC suppressed tumor cell invasion and promoted
mesenchymal-epithelial transition (MET) via suppressing Twist expression. In
vivo, the volume of the tumors in H19-inteference group was significantly
decreased compared to those in the control group of nude mice. Both western-blot
and immunohistochemistry confirmed that a MET phenotype existed in the H19
interference group when compared to control group. These results defined H19 as a
novel prognostic factor for GBC, and indicated that it might play important
regulatory roles in the EMT process.
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