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Enhancement of androgen-dependent transcription and cell proliferation by tributyltin and triphenyltin in human prostate cancer cells.

Abstract：

:Tributyltin (TBT) and triphenyltin (TPT) are known to cause imposex, the superimposing of male genitals on female ones, in some species of gastropods. However, the molecular mechanism of the trialkyltin-induced endocrine dysfunction remains to be elucidated. To clarify the effects of organotin compounds on the activation of androgen receptor (AR)-mediated responses in mammals, a LA16 clone that stably expresses androgen-responsive luciferase reporter gene and proliferates in response to androgen was established from human prostate cancer cell line LNCaP. Stimulation of LA16 cells with 100 nM TBT or 1 nM TPT enhanced both AR-dependent transcription of luciferase gene and cell growth to the same extent as those by 1 nM dihydrotestosterone (DHT). TBT or TPT also enhanced the DNA synthesis and expression of endogenous AR target genes such as prostate specific antigen, but not the expression of AR itself. However, an androgen antagonist, flutamide, did not inhibit the TBT- or TPT-induced AR activation. On the other hand, simultaneous treatment of LA16 cells with DHT and TBT or TPT caused highly enhanced effects on AR activation. These results indicate that trialkyltin compounds have an ability to activate AR-mediated transcription in mammalian cells and suggest that a novel target site other than the ligand-binding site of AR is involved in this activation.

journal_name

Toxicol Appl Pharmacol

journal_title

Toxicology and applied pharmacology

authors

Yamabe Y,Hoshino A,Imura N,Suzuki T,Himeno S

doi

10.1006/taap.2000.9067

subject

Has Abstract

pub_date

2000-12-01 00:00:00

pages

177-84

issue

2

eissn

0041-008X

issn

1096-0333

pii

S0041-008X(00)99067-7

journal_volume

169

pub_type

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