Evidence map›Paper›PMID 22831834›Full record

ArticleJournal of molecular cell biology2013

New therapy targeting differential androgen receptor signaling in prostate cancer stem/progenitor vs. non-stem/progenitor cells.

Soo Ok Lee, Zhifang Ma, Chiuan-Ren Yeh, Jie Luo, Tzu-Hua Lin, Kuo-Pao Lai, Shinichi Yamashita, Liang Liang, Jing Tian, Lei Li and 5 more

RetractedErratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
9.5field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Revisiting the therapeutic potential of tocotrienol.BioFactors (Oxford, England) · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 3 countries.

Soo Ok LeeGeorge Whipple Lab for Cancer Research, Department of Pathology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Zhifang Ma
Chiuan-Ren Yeh
Jie Luo
Tzu-Hua Lin
Kuo-Pao Lai
Shinichi Yamashita
Liang Liang
Jing Tian
Lei Li
Qi Jiang
Chiung-Kuei Huang
Yuanjie Niu
Shuyuan Yeh
Chawnshang Chang
University of Rochester Medical Center · USChina Medical University · TWShanxi Medical University · CN

Funding

Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
Loss of Androgen Receptor Promotes Metastatic Prostate CancerR01CA122840 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2007 to 2011
$1.5M
NCI NIH HHS CA122840NCI NIH HHS CA156700
6 · The paper itself

Abstract

The androgen deprivation therapy (ADT) to systematically suppress/reduce androgens binding to the androgen receptor (AR) has been the standard therapy for prostate cancer (PCa); yet, most of ADT eventually fails leading to the recurrence of castration resistant PCa. Here, we found that the PCa patients who received ADT had increased PCa stem/progenitor cell population. The addition of the anti-androgen, Casodex, or AR-siRNA in various PCa cells led to increased stem/progenitor cells, whereas, in contrast, the addition of functional AR led to decreased stem/progenitor cell population but increased non-stem/progenitor cell population, suggesting that AR functions differentially in PCa stem/progenitor vs. non-stem/progenitor cells. Therefore, the current ADT might result in an undesired expansion of PCa stem/progenitor cell population, which explains why this therapy fails. Using various human PCa cell lines and three different mouse models, we concluded that targeting PCa non-stem/progenitor cells with AR degradation enhancer ASC-J9 and targeting PCa stem/progenitor cells with 5-azathioprine and γ-tocotrienol resulted in a significant suppression of the tumors at the castration resistant stage. This suggests that a combinational therapy that simultaneously targets both stem/progenitor and non-stem/progenitor cells will lead to better therapeutic efficacy and may become a new therapy to battle the PCa before and after castration resistant stages.

Indexed as

Signal TransductionAnimalsAzacitidineCurcuminDecitabineDisease Models, AnimalGene Expression Regulation, NeoplasticHumansMaleMiceNeoplastic Stem CellsOrchiectomyProstatic NeoplasmsReceptors, AndrogenXenograft Model Antitumor AssaysASC-J9 compoundAzacitidineCurcuminDecitabineReceptors, Androgen

Identifiers

PMID22831834
PMCPMC3570051
OpenAlexW2134690947

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.