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In addition, at least 7 other so-called “cryptic” exons (CE1-5, CE1b, and CE9) have been identified in the AR gene. The AR gene is found at Xq11-13 and has 8 canonical exons that encode a modular transcription factor consisting of an N-terminal transactivation domain (NTD, encoded by exon 1), a central DNA binding domain (DBD, exons 2-3), a hinge region harboring the second half of the bipartite nuclear localization signal (NLS, exon 4), and a C-terminal ligand-binding domain (LBD, exons 5-8). In recent years, increased expression of variant transcripts from the AR gene (ARVs) has been shown to represent one such adaptive mechanism. Despite an initial response to ADT, men with prostate cancer invariably progress to an incurable state called castration-resistant prostate cancer (CRPC), thought to occur via therapy-driven adaptive mechanisms that sustain or resurrect an active AR signaling axis in prostate cancer cells. Accordingly, androgen deprivation therapy (ADT), achieved via blockage of androgen production through castration and/or antagonism of AR activity by anti-androgens, forms the cornerstone of endocrine therapy for this disease.
#HOW TO FIND SERUM SERIAL NUMBER ON SPLICE TRIAL DRIVER#
Indeed, AR is considered the key oncogenic driver at all stages of prostate cancer. The AR is widely expressed in many male and female tissues, but the molecular biology of this sex steroid receptor has largely been characterized in studies of the prostate gland, where the AR has critical functions in regulating its development and normal physiology as well as mediating pathology, including cancer development and progression. Development of the male phenotype and adult reproductive function is dependent on a functional AR, while the role of AR in establishing a female phenotype and regulating adult reproductive function appears to be more modulatory than essential. The androgen receptor (AR) is a sex steroid hormone receptor that directly mediates the actions of androgen hormones.
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Collectively, these data provides insight into the potential complexity of AR transcriptional splicing events in breast cancer cell lines and diverse human tissues, thereby establishing a rationale for further exploration of ARVs in breast cancer and other human pathologies. Sequencing of ARV amplicons revealed a single nucleotide substitution within CE3 in lung and placental tissue samples that could be translated as an Ile (ATT)>Val (GTT) substitution in the AR-V7 variant protein.
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In addition, four novel ARVs containing a cryptic exon 9 (CE9) were detected in MDA-MB-453 and VCaP cells. Four ARVs (V1, V3, V7, V9) were detected to some degree in almost all cell lines and tissues. Herein, the expression of five previously identified ARV transcripts with documented transcriptional capacity (AR-V1, -V3, -V4, -V7, and -V9) was examined in 6 breast (MFM223, MDA-MB-453, MDA-MB-231, ZR75.1, MCF-7, T47D), two prostate (VCaP, LNCaP), and one liver (HepG2) cancer cell lines, a human embryonic kidney cell line (HEK293), and a panel of RNAs representing 21 different human tissues. We hypothesised that ARVs are also expressed in breast cancers and other hormone sensitive tissues. Expression of AR splice variants (ARVs) and their role in prostate carcinogenesis has been elucidated in recent studies. AR activity inhibits breast growth and has pleiotropic actions in breast cancer that are subtype-dependent. In particular, the AR plays a critical role in the biology and pathology of the prostate gland. The androgen receptor (AR) is widely expressed in human tissues and has biological function in many male and female organs.