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E2F1 promotes tumor cell invasion and migration through regulating CD147 in prostate cancer
Author(s) -
YuXiang Liang,
Jianming Lü,
Rujun Mo,
He Huang,
Jian Xie,
Funeng Jiang,
Zhengfang Lin,
Yanru Chen,
Yunxiang Wu,
Hongwei Luo,
Zheng Luo,
Weide Zhong
Publication year - 2016
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2016.3364
Subject(s) - e2f1 , cancer research , prostate cancer , cell cycle , biology , oncogene , cancer , chromatin immunoprecipitation , cell growth , epithelial–mesenchymal transition , metastasis , gene expression , gene , biochemistry , genetics , promoter
Increased expression of E2F1 has been reported to be associated with tumor growth and cell survival of prostate cancer (PCa). However, its roles and mechanisms on PCa have not been fully elucidated. The present study found that E2F1 overexpression in PCa tissues was significantly associated with high Gleason score (P=0.01) and advanced pathological stage (P=0.02). In addition, PCa patients with high E2F1 expression more frequently had shorter biochemical recurrence-free survival (P=0.047) than those with low E2F1 expression. Then, we confirmed that the knock-down of E2F1 expression was able to inhibit cell cycle progression, invasion and migration of PCa cell lines in vitro, along with tumor xenograft growth and epithelial-to-mesenchymal transition (EMT) in vivo. Moreover, we identified CD147 as a novel interaction partner for E2F1 through bio-informatic binding site prediction, combined with chromatin immunoprecipitation-PCR (ChIP-PCR) and western blot analysis. Taken together, our data delineate an as yet unrecognized function of E2F1 as enhancer of tumor invasion and migration of PCa via regulating the expression of CD147 in PCa. Importantly, E2F1 may function as a biomarker that can differentiate patients with biochemical recurrent and non-biochemical recurrent disease following radical prostatectomy, highlighting its potential as a therapeutic target.

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