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Cell Biochem Funct. 2008 Jun;26(4):467-77. doi: 10.1002/cbf.1468.

Overexpression of JKTBP1 induces androgen-independent LNCaP cell proliferation through activation of epidermal growth factor-receptor (EGF-R).

Author information

1
Core Facility of Gene Engineered Mouse, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, PR China.

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.

PMID:
18381662
DOI:
10.1002/cbf.1468
[Indexed for MEDLINE]

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