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Overexpression of JKTBP1 induces androgen‐independent LNCaP cell proliferation through activation of epidermal growth factor‐receptor (EGF‐R)
Author(s) -
Wu YongYang,
Li Hong,
Lv XiaoYan,
Wei Qiang,
Li Xiang,
Liu XinYu,
Zhou Qin,
Wei YuQuan
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1468
Subject(s) - lncap , cell growth , prostate cancer , epidermal growth factor , androgen receptor , cancer research , ectopic expression , hyperplasia , prostate , dihydrotestosterone , androgen , biology , endocrinology , medicine , cell culture , cancer , receptor , hormone , biochemistry , genetics
Abstract Heterogenous nuclear ribonucleoprotein D‐like protein (JKTBP) belongs to a new member of hnRNPs. Previous studies implied that JKTBP1 may be associated with the progression of androgen‐independent (AI) prostate cancer. In this study, we generated three stable LNCaP cell lines which expressed exogenous JKTBP1. Furthermore, the effect of ectopic JKTBP1 on the proliferation of LNCaP cells and its mechanism was investigated. We originally found that the ectopic JKTBP1 expression resulted in the proliferation of LNCaP cells in an AI way, as well as inducing the upregulated expression of EGF‐R and prostate‐specific antigen (PSA), but did not influence the expression level of AR. Moreover, AG1478 suppressed the effect of proliferation induced by JKTBP1. In addition, immunohistochemistry showed that JKTBP1 expression was significantly elevated in AI prostate cancer tissues when compared with the androgen‐dependent (AD) prostate cancer and benign prostatic hyperplasia. Our data indicated that overexpression of JKTBP1 in LNCaP cells leads to abnormal cell proliferation and may be involved in the process of AD to AI through induction of EGF‐R expression. Copyright © 2008 John Wiley & Sons, Ltd.