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Chinese Journal of Oncology ; (12): 165-168, 2012.
Article in Chinese | WPRIM | ID: wpr-335320

ABSTRACT

<p><b>OBJECTIVE</b>To explore how NF-κB family members regulate maspin expression in prostate cancer cells.</p><p><b>METHODS</b>The expression of NF-κB subunits and maspin was detected by Western blot analysis in prostate cancer DU145, PC-3, and LNCaP cell lines. RNA interference was performed to analyze whether RelB- or RelA-deletion affectes cell death as well as the expression of NF-κB subunits and maspin. The impact of RelB-silencing in DU145 cells was investigated by flow cytometry. The regulation of RelB on maspin expression in the prostate cancer PC-3 cells was also examined via stable transfection of RelB expression plasmid.</p><p><b>RESULTS</b>RelA, p50, RelB, and p52 were constitutively expressed in androgen-independent prostate cancer DU145 and PC-3 cells, while RelB had the highest expression in DU145 cells. Low expression of maspin was detected in LNCaP and DU145 cells, but elevated expression in PC-3 cells. RelB-silencing in DU145 cells by siRNA interference upregulated the endogenous expression of maspin and induced cell apoptosis (13.3±4.2)%. Overexpression of RelB in PC-3 cells inhibited the endogenous expression of maspin. RelA-silecing had no significant influence on the endogenous expression of maspin.</p><p><b>CONCLUSIONS</b>The classical and alternative NF-κB activitions are sustained in androgen-independent prostate cancer cell lines. The expressions of RelB and maspin are inversely correlated in these cancer cells. The expression of RelB negatively regulates the endogenous expression of maspin, then interferes the cell survival. RelA is not involved in the regulation of maspin expression.</p>


Subject(s)
Humans , Male , Apoptosis , Cell Line, Tumor , Gene Silencing , NF-kappa B , Genetics , Metabolism , NF-kappa B p50 Subunit , Genetics , Metabolism , NF-kappa B p52 Subunit , Genetics , Metabolism , Prostatic Neoplasms , Genetics , Metabolism , Pathology , RNA, Small Interfering , Genetics , Serpins , Metabolism , Transcription Factor RelA , Genetics , Metabolism , Transcription Factor RelB , Genetics , Metabolism , Transfection
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