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M. Fu, C. Wang, A. T. Reutens, J. Wang, R. H. Angeletti, L. Siconolfi-Baez, V. Ogryzko, M. L. Avantaggiati and G. Pestell, “P300 and P300/cAMP-Response ElementBinding Protein-Associated Factor Acetylate the Androgen Receptor at Sites Governing Hormone-Dependent Transactivation,” The Journal of Biological Chemistry, Vol. 275, No. 27, 2000, pp. 20853-20860. doi:10.1074/jbc. M000660200

has been cited by the following article:

• TITLE: Targeting of Androgen Receptor Expression by Andro-miRs as Novel Adjunctive Therapeutics in Prostate Cancer

  AUTHORS: Jey Sabith Ebron, Crystal M. Weyman, Girish C. Shukla

  KEYWORDS: Androgen Receptor; microRNA; 3’ Untranslated Region; Prostate Cancer; Castration-Resistant Prostate Cancer (CRPC); Andro-miR

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.4A, April 29, 2013

  ABSTRACT: Prostate cancer begins as an androgen-responsive disease. However, subsequent accumulation of multiple sequential genetic and epigenetic alterations transforms the disease into an aggressive, castration-resistant prostate cancer (CRPC). The monoallelic Androgen Receptor (AR) is associated with the onset, growth and development of Prostate cancer. The AR is a ligand-dependent transcription factor, and the targeting of androgen- and AR-signaling axis remains the primary therapeutic option for Prostate cancer (PCa) treatment. A durable and functional disruption of AR signaling pathways combining both traditional and novel therapeutics is likely to provide better treatment options for CRPC. Recent work has indicated that expression of AR is modulated at the posttranscriptional level by regulatory miRNAs. Due to a relatively long 3’ untranslated region (UTR) of AR mRNA, the posttranscription expression is likely to be regulated by hundreds of miRNAs in normal as well as in disease state. The main objective of the article is to offer a thought-provoking concept of “andro-miRs” and their potential application in AR gene expression targeting. This new paradigm for targeting constitutively active AR and its tumor specific splicing isoforms using andro-miRs may pave the way for a novel adjunctive therapy and improved treatment of CRPC.