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2017 ; 6
(4
): 834-844
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GOLPH3 induces epithelial-mesenchymal transition via Wnt/?-catenin signaling
pathway in epithelial ovarian cancer
#MMPMID28332316
Sun J
; Yang X
; Zhang R
; Liu S
; Gan X
; Xi X
; Zhang Z
; Feng Y
; Sun Y
Cancer Med
2017[Apr]; 6
(4
): 834-844
PMID28332316
show ga
Golgi phosphoprotein 3 (GOLPH3), a newly recognized oncogene, is associated with
tumor growth, metastasis, and poor prognosis in several types of cancer. However,
its biological role and underlying mechanism in epithelial ovarian cancer (EOC)
remain poorly understood. Here, we found that GOLPH3 was overexpressed in EOC
tissues and cell lines. This overexpression promoted the migration and invasion
of EOC cells. Moreover, GOLPH3 upregulated the expression of
epithelial-mesenchymal transition (EMT) markers, such as N-cadherin and Snail,
and the Wnt/?-catenin-related genes cyclin-D1 and c-Myc, which were restored via
silencing of GOLPH3 expression. Furthermore, the inhibitor and activator of the
Wnt/?-catenin pathway, XAV939 and LiCl, enhanced or decreased, respectively, the
effect of GOLPH3 on EMT, which further confirmed that GOLPH3 promoted EMT
progression via activation of Wnt/?-catenin signaling. In addition, we found that
EDD, the human hyperplastic discs gene, was consistent with GOLPH3 expression and
also promoted the EMT process and activated Wnt/?-catenin signaling. These
findings demonstrate that EDD might be a downstream factor of GOLPH3. Taken
together, our findings demonstrate the existence of a GOLPH3-Wnt/?-catenin-EMT
axis in EOC and provide a new therapeutic target to treat EOC.