Evidence map›Paper›PMID 25132238›Full record

ArticleThe Journal of urology2015

The cistrome and gene signature of androgen receptor splice variants in castration resistant prostate cancer cells.

Ji Lu, Peter E Lonergan, Lucas P Nacusi, Liguo Wang, Lucy J Schmidt, Zhifu Sun, Travis Van der Steen, Stephen A Boorjian, Farhad Kosari, George Vasmatzis and 5 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of urology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Constitutively Active Androgen Receptor in Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. AR Structural Variants and Prostate Cancer.Advances in experimental medicine and biology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Ji LuDepartment of Urology, First Hospital of Jilin University, Changchun, People's Republic of China; Department of Urology, Mayo Clinic, Rochester, Minnesota.
Peter E LonerganDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Lucas P NacusiDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Liguo WangDivision of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota.
Lucy J SchmidtDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Zhifu SunDivision of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota.
Travis Van der SteenDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Stephen A BoorjianDepartment of Urology, Mayo Clinic, Rochester, Minnesota.
Farhad KosariDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
George VasmatzisDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
George G KleeDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota.
Steven P BalkHematology-Oncology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Haojie HuangDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.
Chunxi WangDepartment of Urology, First Hospital of Jilin University, Changchun, People's Republic of China. Electronic address: chunxi_wang@126.com.
Donald J TindallDepartment of Urology, Mayo Clinic, Rochester, Minnesota; Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota. Electronic address: tindall@mayo.edu.
Mayo Clinic · USJilin University · CNHarvard University · US

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Utility of serum and Tissue Biomarkers for Predicting Response to Androgen DeprivP50CA091956 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2001 to 2010
$23.4M
NCI NIH HHS CA091956NCI NIH HHS P30 CA015083NCI NIH HHS P50 CA091956
6 · The paper itself

Abstract

purposeSpliced variant forms of androgen receptor were recently identified in castration resistant prostate cancer cell lines and clinical samples. We identified the cistrome and gene signature of androgen receptor splice variants in castration resistant prostate cancer cell lines and determined the clinical significance of androgen receptor splice variant regulated genes. MATERIALS AND

methodsThe castration resistant prostate cancer cell line 22Rv1, which expresses full-length androgen receptor and androgen receptor splice variants endogenously, was used as the research model. We established 22Rv1-ARFL(-)/ARV(+) and 22Rv1-ARFL(-)/ARV(-) through RNA interference. Chromatin immunoprecipitation coupled with next generation sequencing and microarray techniques were used to identify the cistrome and gene expression profiles of androgen receptor splice variants in the absence of androgen.

resultsAndrogen receptor splice variant binding sites were identified in 22Rv1-ARFL(-)/ARV(+). A gene set was regulated uniquely by androgen receptor splice variants but not by full-length androgen receptor in the absence of androgen. Integrated analysis revealed that some genes were directly modulated by androgen receptor splice variants. Unsupervised clustering analysis showed that the androgen receptor splice variant gene signature differentiated benign from malignant prostate tissue as well as localized prostate cancer from metastatic castration resistant prostate cancer specimens. Some genes that were modulated uniquely by androgen receptor splice variants also correlated with histological grade and biochemical failure.

conclusionsAndrogen receptor splice variants can bind to DNA independent of full-length androgen receptor in the absence of androgen and modulate a unique set of genes that is not regulated by full-length androgen receptor. The androgen receptor splice variant gene signature correlates with disease progression. It distinguishes primary cancer from castration resistant prostate cancer specimens and benign from malignant prostate specimens.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptomeHigh-Throughput Nucleotide SequencingHumansMaleProstatic Neoplasms, Castration-ResistantProtein IsoformsReceptors, AndrogenTumor Cells, CulturedAR protein, humanProtein IsoformsReceptors, Androgenalternative splicingandrogencastration-resistantdisease progressionprostatic neoplasmsreceptorstranscriptome

Identifiers

PMID25132238
PMCPMC4411637
OpenAlexW2059134151

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.