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Mechanisms of the androgen receptor splicing in prostate cancer cells
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Mechanisms of the androgen receptor splicing in prostate cancer cells
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Journal Article
Mechanisms of the androgen receptor splicing in prostate cancer cells
2014
Overview
Prostate tumors develop resistance to androgen deprivation therapy (ADT) by multiple mechanisms, one of which is to express constitutively active androgen receptor (AR) splice variants lacking the ligand-binding domain. AR splice variant 7 (AR-V7, also termed AR3) is the most abundantly expressed variant that drives prostate tumor progression under ADT conditions. However, the molecular mechanism by which AR-V7 is generated remains unclear. In this manuscript, we demonstrated that RNA splicing of AR-V7 in response to ADT was closely associated with
AR
gene transcription initiation and elongation rates. Enhanced
AR
gene transcription by ADT provides a prerequisite condition that further increases the interactions between AR pre-mRNA and splicing factors. Under ADT conditions, recruitment of several RNA splicing factors to the 3′ splicing site for AR-V7 was increased. We identified two RNA splicing enhancers and their binding proteins (U2AF65 and ASF/SF2) that had critical roles in splicing AR pre-mRNA into AR-V7. These data indicate that ADT-induced
AR
gene transcription rate and splicing factor recruitment to AR pre-mRNA contribute to the enhanced AR-V7 levels in prostate cancer cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Alternative Splicing - genetics
/ Animals
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Male
/ Medicine
/ Mice
/ Oncology
/ Prostatic Neoplasms - drug therapy
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - pathology
/ Real-Time Polymerase Chain Reaction
/ Receptors, Androgen - genetics
/ Receptors, Androgen - metabolism
/ Reverse Transcriptase Polymerase Chain Reaction
/ RNA
