Inhibition of androgen receptor transactivation function by adenovirus type 12 E1A undermines prostate cancer cell survival

The Prostate
Dawei LiDaiqing Liao

Abstract

Mutations or truncation of the ligand-binding domain (LBD) of androgen receptor (AR) underlie treatment resistance for prostate cancer (PCa). Thus, targeting the AR N-terminal domain (NTD) could overcome such resistance. Luciferase reporter assays after transient transfection of various DNA constructs were used to assess effects of E1A proteins on AR-mediated transcription. Immunofluorescence microscopy and subcellular fractionation were applied to assess intracellular protein localization. Immunoprecipitation and mammalian two-hybrid assays were used to detect protein-protein interactions. qRT-PCR was employed to determine RNA levels. Western blotting was used to detect protein expression in cells. Effects of adenoviruses on prostate cancer cell survival were evaluated with CellTiter-Glo assays. Adenovirus 12 E1A (E1A12) binds specifically to the AR. Interestingly, the full-length E1A12 (266 aa) preferentially binds to full-length AR, while the small E1A12 variant (235 aa) interacts more strongly with AR-V7. E1A12 promotes AR nuclear translocation, likely through mediating intramolecular AR NTD-LBD interactions. In the nucleus, AR and E1A12 co-expression in AR-null PCa cells results in E1A12 redistribution from nuclear foci co...Continue Reading

References

Apr 16, 1998·Proceedings of the National Academy of Sciences of the United States of America·P AarnisaloO A Jänne
Nov 21, 1998·The Journal of Biological Chemistry·K FrønsdalF Saatcioglu
Mar 29, 2000·The Journal of Biological Chemistry·E P RogakouW M Bonner
Dec 28, 2002·Journal of Virology·Bas van BreukelenPeter C van der Vliet
Jan 2, 2004·Nature Medicine·Charlie D ChenCharles L Sawyers
Mar 24, 2004·Proceedings of the National Academy of Sciences of the United States of America·Paul L ShafferDaniel T Gewirth
Apr 26, 2005·Proceedings of the National Academy of Sciences of the United States of America·Xianwang MengPaul G Walfish
Jan 7, 2006·Cancer Research·Leen CallewaertFrank Claessens
Mar 2, 2006·Molecular and Cellular Biology·Kathryn A O'DonnellChi V Dang
Nov 10, 2006·Proceedings of the National Academy of Sciences of the United States of America·Karen I ZellerChia-Lin Wei
Jun 15, 2007·Molecular Therapy : the Journal of the American Society of Gene Therapy·Naseruddin HötiRonald Rodriguez
Aug 5, 2008·Current Opinion in Pharmacology·Yu ChenHoward I Scher
May 28, 2009·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Gerhardt AttardJohann S de Bono
Aug 5, 2009·Proceedings of the National Academy of Sciences of the United States of America·Josephine C FerreonPeter E Wright
Apr 20, 2010·Lancet·Howard I ScherUNKNOWN Prostate Cancer Foundation/Department of Defense Prostate Cancer Clinical Trials Consortium
Jun 29, 2010·Cancer Cell·Barry S TaylorWilliam L Gerald
Jul 21, 2010·The Journal of Clinical Investigation·Shihua SunStephen R Plymate
Mar 5, 2011·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Gerhardt AttardJohann S de Bono
Jul 23, 2011·Endocrine-related Cancer·Scott M Dehm, Donald J Tindall
Jul 29, 2011·Methods in Molecular Biology·Elizabeth M Wilson
Aug 30, 2011·Molecular and Cellular Endocrinology·Dennis J van de WijngaartGuido Jenster

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

© 2022 Meta ULC. All rights reserved