Evidence map›Paper›PMID 21258401›Full record

ArticleOncogene2011

IL-6 promotes prostate tumorigenesis and progression through autocrine cross-activation of IGF-IR.

A Rojas, G Liu, I Coleman, P S Nelson, M Zhang, R Dash, P B Fisher, S R Plymate, J D Wu

Abstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
7.6field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026
    Article
  5. Review
  6. JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

25 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

9 authors at 4 institutions in 1 country.

A RojasDepartment of Medicine, University of Washington, Seattle, WA 98104, USA.
G Liu
I Coleman
P S Nelson
M Zhang
R Dash
P B Fisher
S R Plymate
J D Wu
University of Washington · USFred Hutch Cancer Center · USVirginia Commonwealth University · USSeattle University · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI John Kyung Lee · 2002 to 2026
$58.1M
Transmembrane Proteases and Prostate CarcinogenesisP01CA085859 · NCI · UNIVERSITY OF WASHINGTON · PI VESSELLA, ROBERT LOUIS · 2002 to 2013
$21.2M
Translational Applications of mda-7/IL-24 in CancerP01CA104177 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2005 to 2009
$6.5M
MDA-7: Novel Cancer Therapeutic GeneR01CA097318 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2002 to 2012
$2.8M
Targeting MIC shedding to revive host NKG2D-mediated immune response in prostateR01CA149405 · NCI · UNIVERSITY OF WASHINGTON · PI WU, JENNIFER D · 2010 to 2014
$1.5M
Modeling MIC Shedding in Prostate Cancer ProgressionK01CA116002 · NCI · UNIVERSITY OF WASHINGTON · PI WU, JENNIFER D · 2005 to 2009
$698k
NCI NIH HHS 1K01CA116002NCI NIH HHS 1R01CA149405NCI NIH HHS K01 CA116002NCI NIH HHS P01 CA085859NCI NIH HHS P01 CA104177NCI NIH HHS P50 CA097186NCI NIH HHS P50-CA097186NCI NIH HHS R01 CA097318NCI NIH HHS R01 CA149405
6 · The paper itself

Abstract

As an established mediator of inflammation, interleukin-6 (IL-6) is implicated to facilitate prostate cancer progression to androgen independence through transactivation of the androgen receptor. However, whether IL-6 has a causative role in de novo prostate tumorigenesis was never investigated. We now provide the first evidence that IL-6 can induce tumorigenic conversion and further progression to an invasive phenotype of non-tumorigenic benign prostate epithelial cells. Moreover, we find that paracrine IL-6 stimulates the autocrine IL-6 loop and autocrine activation of insulin-like type I growth factor receptor (IGF-IR) to confer the tumorigenic property and also that activation of signal transducer and activator of transcription 3 (STAT3) is critical in these processes. Inhibition of STAT3 activation or IGF-IR signaling suppresses IL-6-mediated malignant conversion and the associated invasive phenotype. Inhibition of STAT3 activation suppresses IL-6-induced upregulation of IGF-IR and its ligands, namely IGF-I and IGF-II. These findings indicate that IL-6 signaling cooperates with IGF-IR signaling in the prostate microenvironment to promote prostate tumorigenesis and progression to aggressiveness. Our findings suggest that STAT3 and IGF-IR may represent potential effective targets for prevention or treatment of prostate cancer.

Indexed as

Autocrine CommunicationCell LineCell Transformation, NeoplasticDisease ProgressionEpithelial CellsEpithelial-Mesenchymal TransitionHumansInterleukin-6MaleNeoplasm InvasivenessProstateProstatic NeoplasmsReceptor, IGF Type 1Signal TransductionSTAT3 Transcription FactorTranscriptional ActivationInterleukin-6Receptor, IGF Type 1STAT3 Transcription Factor

Identifiers

PMID21258401
PMCPMC3112005
OpenAlexW2048601897

What OpenQuestion holds

Textmetadata
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.