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Golgi phosphoprotein 3 expression predicts poor prognosis in patients with prostate cancer undergoing radical prostatectomy

Authors :
Xing-hua Gao
Feng Guo
Yan-lin Wu
Longyang Zhang
Source :
Molecular Medicine Reports. 12:1298-1304
Publication Year :
2012
Publisher :
Spandidos Publications, 2012.

Abstract

Golgi phosphoprotein 3 (GOLPH3) has recently been implicated as an oncogene involved in the development of carcinoma in a number of organs. The expression of GOLPH3 in prostate cancer (PCa) tissues was investigated in the present study. Human PC-3 and LNCaP PCa cell lines were analyzed in order to assess whether silencing of GOLPH3 expression affects cell vitality, migration and invasion, in vitro. An immunohistochemistry analysis was performed in order to measure the expression of GOLPH3 in samples from 117 patients with PCa and from 50 patients with benign prostatic hyperplasia (BPH). Associations between GOLPH3 expression and clinicopathological parameters, such as overall survival, were assessed. GOLPH3 expression was shown to be significantly greater in PCa tissues than in BPH tissues. GOLPH3 expression was positively correlated with Gleason score (P=0.031), tumor stage (T stage; P=0.020) and lymph node status (P=0.013), in patients with PCa. Biochemical recurrence-free survival (serum prostate-specific antigen-based) and overall survival, were reduced in patients with GOLPH3-positive PCa. A multivariate analysis indicated that GOLPH3 expression was an independent predictor of biochemical recurrence-free survival [hazard ratio (HR), 2.943; 95% confidence interval (CI), 1.190-5.521; P=0.028], and of overall survival (HR, 4.371; 95% CI, 2.045-7.109; P=0.014). Transfection with GOLPH3‑targeted small interfering RNA reduced the capability of PC-3 and LNCaP cell lines to proliferate, migrate and invade in vitro, compared with the controls. The level of GOLPH3 expression in radical prostatectomy samples may be useful for predicting biochemical recurrence-free survival and overall survival in patients with PCa.

Details

ISSN :
17913004 and 17912997
Volume :
12
Database :
OpenAIRE
Journal :
Molecular Medicine Reports
Accession number :
edsair.doi.dedup.....8ff184ccc18f04b517c05140e6dbfdeb