Abstract:
:This study was performed to prove our hypothesis that the metabolite(s) of polycyclic aromatic hydrocarbons (PAHs) caused the activation or phosphorylation of p53 via DNA damage to suppress the liver X receptor (LXR)-mediated signal transductions as a probably more direct mechanism. We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53. The exogenous expression of wild-type p53 suppressed the LXR-mediated trans-activation in Hep3B cells. The expression of mRNA for ATP binding cassette A1 was suppressed by MC and Dox in HepG2 cells. The protein expression of retinoid X receptor (RXR), a partner of LXR to form a heterodimer, was suppressed by MC and Dox in HepG2 cells.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Iwano S,Shibahara N,Saito T,Kamataki Tdoi
10.1016/j.febslet.2006.01.009keywords:
subject
Has Abstractpub_date
2006-02-06 00:00:00pages
890-3issue
3eissn
0014-5793issn
1873-3468pii
S0014-5793(06)00042-1journal_volume
580pub_type
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