Evidence map›Paper›PMID 15688010›Full record

ArticleOncogene2005

A SOCS-1 peptide mimetic inhibits both constitutive and IL-6 induced activation of STAT3 in prostate cancer cells.

Lawrence O Flowers, Prem S Subramaniam, Howard M Johnson

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.4field-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

60 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. SOCS1 Inhibits IL-6-Induced CD155 Overexpression in Lung Adenocarcinoma.International journal of molecular sciences · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. ReducedBiomedicines · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

3 authors at 2 institutions in 1 country.

Lawrence O FlowersDepartment of Microbiology and Cell Science, University of Florida, Gainesville, FL 32611, USA.
Prem S Subramaniam
Howard M Johnson
University of Florida · USScripps Research Institute · US

Funding

Study of gamma interferon agonists/mimeticsR01AI056152 · NIAID · UNIVERSITY OF FLORIDA · PI JOHNSON, HOWARD M · 2003 to 2012
$2.9M
Study of gamma interferon agonists/mimeticsR56AI056152 · NIAID · UNIVERSITY OF FLORIDA · PI JOHNSON, HOWARD M · 2007 to 2007
$366k
NIAID NIH HHS AI56152
6 · The paper itself

Abstract

Prostate cancer is the second highest cause of cancer-related deaths of men in the US. Signal transducers and activators of transcription (STATs) proteins are a small family of latent cytoplasmic transcription factors that act downstream of Janus kinase (JAK) activation and mediate intracellular signaling from a wide variety of cytokines, growth factors, and hormones. Aberrant activation of STAT3 has been implicated in the progression of many human carcinomas, including prostate cancer. Previously, we have characterized a novel tyrosine kinase inhibitor peptide, Tkip, that is a mimetic of suppressor of cytokine signaling 1 (SOCS-1). Similar to SOCS-1, Tkip binds to the autophosphorylation site of JAK2 and inhibits phosphorylation of STAT1alpha. In this study, we determined the inhibitory effects of Tkip on the human prostate cancer cell lines DU145 and LNCaP. Tkip inhibited cellular proliferation of both DU145 and LNCaP cells, with a slightly greater antiproliferative effect on DU145 cells. Cell cycle analysis using flow cytometry showed Tkip blockage of progression into the S phase of the cell cycle. Tkip also inhibited constitutive (DU145) and IL-6-induced (LNCaP) activation of STAT3, consistent with the fact that STAT3 activation is mediated by JAK2. Tkip also slightly reduced the levels of cyclin D1, an important regulator of cell cycle progression into S phase, in DU145 and LNCaP cancer cell lines. These data describe a potentially important therapeutic that targets both constitutive and IL-6-induced STAT3 activation in human prostate cancer cell lines.

Indexed as

Amino Acid SequenceCell DivisionCell Line, TumorDNA-Binding ProteinsHumansInterleukin-6Intracellular Signaling Peptides and ProteinsJanus Kinase 2MaleMolecular Sequence DataPeptide FragmentsProstatic NeoplasmsProtein-Tyrosine KinasesProto-Oncogene ProteinsRepressor ProteinsSTAT3 Transcription FactorDNA-Binding ProteinsInterleukin-6Intracellular Signaling Peptides and ProteinsJAK2 protein, humanJanus Kinase 2Peptide FragmentsProtein-Tyrosine KinasesProto-Oncogene ProteinsRepressor ProteinsSOCS1 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTrans-Activators

Identifiers

PMID15688010
OpenAlexW2079603698

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.