Abstract:
:Lipopolysaccharide (LPS)-induced TLR4-NF-(K)B signaling plays an important role in the development of prostatic tumors from chronic bacterial prostatic infection. Although many studies support the role of selenium in protecting against the development of prostate cancer secondary to chronic prostatitis, the mechanism of action remains unclear. The aim of our study was to investigate whether selenium inhibits the LPS-induced TLR4 signaling pathway in human prostate cancer PC3 cells. Using real-time quantitative PCR and ELISA analysis, we found that pretreatment with selenium (0.5-5uM) inhibited the LPS-induced expression of TGFbeta(1) and VEGF and production of these cytokines and IL-6 by PC3 cells, but did not alter the expression of TLR4 mRNA. Further experiments using Western blot showed that selenium at 3 and 5uM significantly inhibited the translocation of the NF-(K)B p65 subunit to the nucleus in LPS-stimulated PC3 cells. Our results suggest that low doses of selenium may protect the prostate from prostatitis-induced cancer by inhibiting nuclear translocation of the NF-(K)B and the subsequent production of the immunosuppressive cytokine TGFbeta(1), proangiogenic factor VEGF and pro-inflammatory factor IL-6.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
Pei Z,Li H,Guo Y,Jin Y,Lin Ddoi
10.1016/j.intimp.2009.09.020subject
Has Abstractpub_date
2010-01-01 00:00:00pages
50-6issue
1eissn
1567-5769issn
1878-1705pii
S1567-5769(09)00312-9journal_volume
10pub_type
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