Evidence map›Paper›PMID 23012352›Full record

ArticleThe Journal of biological chemistry2012

Targeting the unique methylation pattern of androgen receptor (AR) promoter in prostate stem/progenitor cells with 5-aza-2'-deoxycytidine (5-AZA) leads to suppressed prostate tumorigenesis.

Jing Tian, Soo Ok Lee, Liang Liang, Jie Luo, Chiung-Kuei Huang, Lei Li, Yuanjie Niu, Chawnshang Chang

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
4.9field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Dysregulated Transcriptional Control in Prostate Cancer.International journal of molecular sciences · 2019
    Review
  10. Review
  11. Key actors in cancer therapy: epigenetic modifiers.Turkish journal of biology = Turk biyoloji dergisi · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Epigenetics in cancer stem cells.Molecular cancer · 2017
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 3 countries.

Jing TianChawnshang Chang Sex Hormone Research Center, Tianjin Institute of Urology, Tianjin Medical University, Tianjin 300211, China.
Soo Ok Lee
Liang Liang
Jie Luo
Chiung-Kuei Huang
Lei Li
Yuanjie Niu
Chawnshang Chang
University of Rochester Medical Center · USTianjin Medical University · CNChina Medical University Hospital · TWFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

New Mice Models for Studies of Androgen Receptor in Prostate CancerR01CA127300 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2008 to 2012
$1.6M
NCI NIH HHS CA127300NCI NIH HHS R01 CA127300
6 · The paper itself

Abstract

Androgen receptor (AR) expression surveys found that normal prostate/prostate cancer (PCa) stem/progenitor cells, but not embryonic or mesenchymal stem cells, expressed little AR with high methylation in the AR promoter. Mechanism dissection revealed that the differential methylation pattern in the AR promoter could be due to differential expression of methyltransferases and binding of methylation binding protein to the AR promoter region. The low expression of AR in normal prostate/PCa stem/progenitor cells was reversed after adding 5-aza-2'-deoxycytidine, a demethylating agent, which could then lead to decreased stemness and drive cells into a more differentiated status, suggesting that the methylation in the AR promoter of prostate stem/progenitor cells is critical not only in maintaining the stemness but also critical in protection of cells from differentiation. Furthermore, induced AR expression, via alteration of its methylation pattern, led to suppression of the self-renewal/proliferation of prostate stem/progenitor cells and PCa tumorigenesis in both in vitro assays and in vivo orthotopic xenografted mouse studies. Taken together, these data prove the unique methylation pattern of AR promoter in normal prostate/PCa stem/progenitor cells and the influence of AR on their renewal/proliferation and differentiation. Targeting PCa stem/progenitor cells with alteration of methylated AR promoter status might provide a new potential therapeutic approach to battle PCa because the PCa stem/progenitor cells have high tumorigenicity.

Indexed as

Promoter Regions, GeneticAnimalsAntimetabolites, AntineoplasticAzacitidineCell DifferentiationCell Line, TumorCell ProliferationCell Transformation, NeoplasticDecitabineDNA MethylationDNA, NeoplasmGene Expression Regulation, NeoplasticHumansMaleMiceNeoplasm ProteinsAntimetabolites, AntineoplasticAzacitidineDecitabineDNA, NeoplasmNeoplasm ProteinsReceptors, Androgen

Identifiers

PMID23012352
PMCPMC3501037
OpenAlexW1982814339

What OpenQuestion holds

Textmetadata
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.