Ligand-Independent Androgen Receptor Variants Derived from Splicing of Cryptic Exons Signify Hormone-Refractory Prostate Cancer
Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel...
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| Published in | Cancer research (Chicago, Ill.) Vol. 69; no. 1; pp. 16 - 22 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Philadelphia, PA
American Association for Cancer Research
01.01.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0008-5472 1538-7445 1538-7445 |
| DOI | 10.1158/0008-5472.CAN-08-2764 |
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| Abstract | Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered seven AR variant transcripts lacking the reading frames for the ligand-binding domain due to splicing of “intronic” cryptic exons to the upstream exons encoding the AR DNA-binding domain. We focused on the two most abundantly expressed variants, AR-V1 and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA showed an average 20-fold higher expression in HRPC (n = 25) when compared with hormone-naive PCa (n = 82; P < 0.0001). Among the hormone-naive PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (P = 0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone-naive PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa. [Cancer Res 2009;69(1):16–22] |
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| AbstractList | Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered seven AR variant transcripts lacking the reading frames for the ligand-binding domain due to splicing of “intronic” cryptic exons to the upstream exons encoding the AR DNA-binding domain. We focused on the two most abundantly expressed variants, AR-V1 and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA showed an average 20-fold higher expression in HRPC (n = 25) when compared with hormone-naive PCa (n = 82; P < 0.0001). Among the hormone-naive PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (P = 0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone-naive PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa. [Cancer Res 2009;69(1):16–22] Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone refractory prostate cancer (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered 7 AR variant transcripts lacking the reading frames for the ligand-binding domain, due to splicing of “intronic” cryptic exons to the upstream exons encoding the AR DNA binding domain. We focused on the two most abundantly expressed variants, AR-V1, and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA demonstrated an average 20-fold higher expression in HRPC (n=25) when compared to hormone naïve PCa (n=82) (p<0.0001). Among the hormone naïve PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (p=0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone naïve PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa. Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered seven AR variant transcripts lacking the reading frames for the ligand-binding domain due to splicing of "intronic" cryptic exons to the upstream exons encoding the AR DNA-binding domain. We focused on the two most abundantly expressed variants, AR-V1 and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA showed an average 20-fold higher expression in HRPC (n = 25) when compared with hormone-naive PCa (n = 82; P < 0.0001). Among the hormone-naive PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (P = 0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone-naive PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa. Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered seven AR variant transcripts lacking the reading frames for the ligand-binding domain due to splicing of "intronic" cryptic exons to the upstream exons encoding the AR DNA-binding domain. We focused on the two most abundantly expressed variants, AR-V1 and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA showed an average 20-fold higher expression in HRPC (n = 25) when compared with hormone-naive PCa (n = 82; P < 0.0001). Among the hormone-naive PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (P = 0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone-naive PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa.Suppression of androgen production and function provides palliation but not cure in men with prostate cancer (PCa). Therapeutic failure and progression to hormone-refractory PCa (HRPC) are often accompanied by molecular alterations involving the androgen receptor (AR). In this study, we report novel forms of AR alteration that are prevalent in HRPC. Through in silico sequence analysis and subsequent experimental validation studies, we uncovered seven AR variant transcripts lacking the reading frames for the ligand-binding domain due to splicing of "intronic" cryptic exons to the upstream exons encoding the AR DNA-binding domain. We focused on the two most abundantly expressed variants, AR-V1 and AR-V7, for more detailed analysis. AR-V1 and AR-V7 mRNA showed an average 20-fold higher expression in HRPC (n = 25) when compared with hormone-naive PCa (n = 82; P < 0.0001). Among the hormone-naive PCa, higher expression of AR-V7 predicted biochemical recurrence following surgical treatment (P = 0.012). Polyclonal antibodies specific to AR-V7 detected the AR-V7 protein frequently in HRPC specimens but rarely in hormone-naive PCa specimens. AR-V7 was localized in the nuclei of cultured PCa cells under androgen-depleted conditions, and constitutively active in driving the expression of canonical androgen-responsive genes, as revealed by both AR reporter assays and expression microarray analysis. These results suggest a novel mechanism for the development of HRPC that warrants further investigation. In addition, as expression markers for lethal PCa, these novel AR variants may be explored as potential biomarkers and therapeutic targets for advanced PCa. |
| Author | Luo, Jun Bova, G. Steven Humphreys, Elizabeth Partin, Alan W. Isharwal, Sumit Dunn, Thomas A. Veltri, Robert W. Wei, Shuanzeng Vessella, Robert L. Hu, Rong Isaacs, William B. Han, Misop |
| AuthorAffiliation | 2 Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD 4 Department of Urology, University of Washington and the Puget Sound VA Medical Center, Seattle, Washington 3 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 1 Department of Urology, The Johns Hopkins University School of Medicine, Baltimore, MD |
| AuthorAffiliation_xml | – name: 4 Department of Urology, University of Washington and the Puget Sound VA Medical Center, Seattle, Washington – name: 2 Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD – name: 1 Department of Urology, The Johns Hopkins University School of Medicine, Baltimore, MD – name: 3 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD |
| Author_xml | – sequence: 1 givenname: Rong surname: Hu fullname: Hu, Rong – sequence: 2 givenname: Thomas A. surname: Dunn fullname: Dunn, Thomas A. – sequence: 3 givenname: Shuanzeng surname: Wei fullname: Wei, Shuanzeng – sequence: 4 givenname: Sumit surname: Isharwal fullname: Isharwal, Sumit – sequence: 5 givenname: Robert W. surname: Veltri fullname: Veltri, Robert W. – sequence: 6 givenname: Elizabeth surname: Humphreys fullname: Humphreys, Elizabeth – sequence: 7 givenname: Misop surname: Han fullname: Han, Misop – sequence: 8 givenname: Alan W. surname: Partin fullname: Partin, Alan W. – sequence: 9 givenname: Robert L. surname: Vessella fullname: Vessella, Robert L. – sequence: 10 givenname: William B. surname: Isaacs fullname: Isaacs, William B. – sequence: 11 givenname: G. Steven surname: Bova fullname: Bova, G. Steven – sequence: 12 givenname: Jun surname: Luo fullname: Luo, Jun |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21883664$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19117982$$D View this record in MEDLINE/PubMed |
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| CODEN | CNREA8 |
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| Keywords | Treatment resistance Urinary system disease Genetic variability Prostate disease Androgen Splicing Hormone therapy Ligand Genotype Malignant tumor Cryptic Variant Exon Hormonoindependence Sex steroid hormone Male genital diseases Prostate cancer Cancer |
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| SubjectTerms | Alternative Splicing Antineoplastic agents Biological and medical sciences Cloning, Molecular Exons Gynecology. Andrology. Obstetrics Humans Ligands Male Male genital diseases Medical sciences Neoplasms, Hormone-Dependent - genetics Neoplasms, Hormone-Dependent - metabolism Nephrology. Urinary tract diseases Open Reading Frames Pharmacology. Drug treatments Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Protein Biosynthesis Protein Isoforms Receptors, Androgen - biosynthesis Receptors, Androgen - genetics Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| Title | Ligand-Independent Androgen Receptor Variants Derived from Splicing of Cryptic Exons Signify Hormone-Refractory Prostate Cancer |
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