Evidence map›Paper›PMID 23928703›Full record

ArticleCell death & disease2013

Anti-androgen receptor ASC-J9 versus anti-androgens MDV3100 (Enzalutamide) or Casodex (Bicalutamide) leads to opposite effects on prostate cancer metastasis via differential modulation of macrophage infiltration and STAT3-CCL2 signaling.

T-H Lin, K Izumi, S O Lee, W-J Lin, S Yeh, C Chang

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Sequential Enzalutamide-Docetaxel Versus Abiraterone-Docetaxel Therapy in Castration-Resistant Prostate Cancer: A Subanalysis of the ENABLE Study.International journal of urology : official journal of the Japanese Urological Association · 2026
    Trial
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  12. Review
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  18. mMolecular therapy. Nucleic acids · 2022
    Article
  19. Focus on the tumor microenvironment: A seedbed for neuroendocrine prostateFrontiers in cell and developmental biology · 2022
    Review
  20. AR Structural Variants and Prostate Cancer.Advances in experimental medicine and biology · 2022
    Article

33 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

T-H LinGeorge Whipple Lab for Cancer Research, University of Rochester Medical Center, Rochester, NY 14642, USA.
K Izumi
S O Lee
W-J Lin
S Yeh
C Chang
University of Rochester Medical Center · USChina Medical University · TW

Funding

Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS CA156700NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Despite androgen deprivation therapy (ADT) suppression of prostate cancer (PCa) growth, its overall effects on PCa metastasis remain unclear. Using human (C4-2B/THP1) and mouse (TRAMP-C1/RAW264.7) PCa cells-macrophages co-culture systems, we found currently used anti-androgens, MDV3100 (enzalutamide) or Casodex (bicalutamide), promoted macrophage migration to PCa cells that consequently led to enhanced PCa cell invasion. In contrast, the AR degradation enhancer, ASC-J9, suppressed both macrophage migration and subsequent PCa cell invasion. Mechanism dissection showed that Casodex/MDV3100 reduced the AR-mediated PIAS3 expression and enhanced the pSTAT3-CCL2 pathway. Addition of CCR2 antagonist reversed the Casodex/MDV3100-induced macrophage migration and PCa cell invasion. In contrast, ASC-J9 could regulate pSTAT3-CCL2 signaling using two pathways: an AR-dependent pathway via inhibiting PIAS3 expression and an AR-independent pathway via direct inhibition of the STAT3 phosphorylation/activation. These findings were confirmed in the in vivo mouse model with orthotopically injected TRAMP-C1 cells. Together, these results may raise the potential concern about the currently used ADT with anti-androgens that promotes PCa metastasis and may provide some new and better therapeutic strategies using ASC-J9 alone or a combinational therapy that simultaneously targets androgens/AR signaling and PIAS3-pSTAT3-CCL2 signaling to better battle PCa growth and metastasis at castration-resistant stage.

Indexed as

Androgen AntagonistsAndrogen Receptor AntagonistsAnilidesAnimalsAntineoplastic AgentsBenzamidesCell MovementChemokine CCL3Coculture TechniquesCurcuminHumansMacrophagesMaleMiceNeoplasm MetastasisNitrilesAndrogen AntagonistsAndrogen Receptor AntagonistsAnilidesAntineoplastic AgentsASC-J9 compoundBenzamidesbicalutamideCCL3 protein, humanChemokine CCL3CurcuminenzalutamideNitrilesPhenylthiohydantoinSTAT3 Transcription FactorTosyl Compounds

Identifiers

PMID23928703
PMCPMC3763432
OpenAlexW2014556566

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.