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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Cancer+Res
2016 ; 6
(11
): 2651-2660
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Long non-coding RNA CCAT2 promotes gastric cancer proliferation and invasion by
regulating the E-cadherin and LATS2
#MMPMID27904778
Wang YJ
; Liu JZ
; Lv P
; Dang Y
; Gao JY
; Wang Y
Am J Cancer Res
2016[]; 6
(11
): 2651-2660
PMID27904778
show ga
Dysregulation of long non-coding RNAs (lncRNAs) play important roles in tumor
development and progression. The long non-coding RNA CCAT2 has been identified to
be up-regulated in gastric cancer (GC). However, the detailed molecular mechanism
of CCAT2 involved in GC progression is still unknown. The aim of this study was
to explore the expression and role of CCAT2 in GC progression. In the study, the
expression levels of CCAT2 were significantly up-regulated in 108 cases GC
tissues compared with adjacent non-tumor tissues by qRT-PCR analysis. Higher
CCAT2 expression was correlated with tumor size, lymph node metastasis and Tumor
Node Metastasis (TNM) stage in GC patients. Multivariate analysis showed that
lymph node metastasis, TNM stage and the expression of CCAT2 were independent
prognostic indicator for disease-free survival (DFS) and the over survival time
(OS) for GC patients. Further function analysis demonstrated that knockdown of
CCAT2 inhibited the cell migration and invasion, whereas, the overexpression of
CCAT2 showed the opposite results in GC cells. Our results also demonstrated that
CCAT2 promoted the GC cells epithelial-mesenchymal transition (EMT) by
downregulated the E-cadherin expression and upregulated the ZEB2, Vimentin and
N-cadherin expression. Moreover, RNA immunoprecipitation (RIP) and Chromatin
immunoprecipitation (ChIP) revealed that CCAT2 interacted with EZH2 and regulated
the E-cadherin and LATS2 expression. Thus, our results demonstrated that CCAT2
functioned as an oncogene in GC and was involved in gastric cancer progression.
Targeting CCAT2 might be a potential therapeutic target for GC.