RETRACTED ARTICLE: Liver X receptors constrain tumor development and metastasis dissemination in PTEN-deficient prostate cancer

Anthony Alioui, Julie Dufour, Valerio Leoni, Anke Loregger, Martina Moeton, Luigi Iuliano, Chiara Zerbinati, Amandine Septier, Pierre Val, Allan Fouache, Vincenzo Russo, David H. Volle, Jean-Marc A. Lobaccaro (), Noam Zelcer and Silvère Baron ()
Additional contact information
Anthony Alioui: Université Clermont Auvergne, Génétique Reproduction et Développement
Julie Dufour: Université Clermont Auvergne, Génétique Reproduction et Développement
Valerio Leoni: Hospital of Varese
Anke Loregger: Academic Medical Center
Martina Moeton: Academic Medical Center
Luigi Iuliano: Sapienza University of Rome
Chiara Zerbinati: Sapienza University of Rome
Amandine Septier: Université Clermont Auvergne, Génétique Reproduction et Développement
Pierre Val: Université Clermont Auvergne, Génétique Reproduction et Développement
Allan Fouache: Université Clermont Auvergne, Génétique Reproduction et Développement
Vincenzo Russo: San Raffaele Scientific Institute
David H. Volle: Université Clermont Auvergne, Génétique Reproduction et Développement
Jean-Marc A. Lobaccaro: Université Clermont Auvergne, Génétique Reproduction et Développement
Noam Zelcer: Academic Medical Center
Silvère Baron: Université Clermont Auvergne, Génétique Reproduction et Développement

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Advanced prostate cancer (PCa) is a clinical challenge as no curative therapeutic is available. In this context, a better understanding of metastasis and resistance mechanisms in PCa is an important issue. As phosphatase and tensin homolog (PTEN) loss is the most common genetic lesion in such cancer, we investigate human data sets for mechanisms that can constrain cancer evolution in this setting. Here we report a liver X receptor (LXR) signature, which tightly correlates with PTEN loss, in PCa. Accordingly, the LXR pathway is deregulated in prostate carcinomas in Pten-null mice. Genetic ablation of LXRs in Pten-null mice, exacerbates PCa invasiveness and metastatic dissemination, which involves mesenchymal transition and accumulation of matrix metalloproteinases. Mechanistically, PTEN deletion governed LXR transcriptional activity through deregulation of cholesterol de novo synthesis, resulting in accumulation of endogenous LXR ligands. Our study therefore reveals a functional circuit linking PTEN and LXR, and highlights LXRs as metabolic gatekeepers that are able to constrain PCa progression.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-017-00508-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00508-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-017-00508-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().