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Inhibition of mammary carcinoma cell growth by RXR is mediated by the receptor's oligomeric switch.

Abstract：

:Ligands that activate the nuclear receptor retinoid X receptor (RXR) display potent anticarcinogenic activities, but the mechanisms by which these compounds inhibit carcinoma cell growth are poorly understood. While RXR can regulate gene expression due to its intrinsic ligand-activated transcription function, this receptor can also regulate transcription by functioning as a ligand-controlled DNA architectural factor. It was thus reported that apo-RXR self-associates into tetramers and that each dimer within these tetramers can separately bind to an RXR response element. Hence, DNA binding by RXR tetramers may bring distant genomic regions into close physical proximity. As ligand binding induces the dissociation of RXR tetramers into dimers, it can alter gene expression by modulating the DNA architecture. Here, we show that inhibition of mammary carcinoma cell growth by RXR ligands stems from the ability of these compounds to regulate the oligomeric state of RXR and is independent of the direct intrinsic transcriptional activity of the receptor. The data suggest that compounds that trigger dissociation of RXR tetramers may comprise a novel class of anticarcinogenic agents.

journal_name

J Mol Biol

journal_title

Journal of molecular biology

authors

Yasmin R,Kannan-Thulasiraman P,Kagechika H,Dawson MI,Noy N

doi

10.1016/j.jmb.2010.02.030

subject

Has Abstract

pub_date

2010-04-16 00:00:00

pages

1121-31

issue

5

eissn

0022-2836

issn

1089-8638

pii

S0022-2836(10)00195-6

journal_volume

397

pub_type

杂志文章

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