Evidence map›Paper›PMID 20233902›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2010

Sulforaphane inhibits constitutive and interleukin-6-induced activation of signal transducer and activator of transcription 3 in prostate cancer cells.

Eun-Ryeong Hahm, Shivendra V Singh

Open access · hybridAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 68 citations in OpenAlex.

  1. Prevention of Carcinogen-Induced Oral Cancer by Sulforaphane.Cancer prevention research (Philadelphia, Pa.) · 2016
    Trial
  2. Article
  3. Review
  4. Review
  5. Mechanistic review of sulforaphane as a chemoprotective agent in bladder cancer.American journal of clinical and experimental urology · 2023
    Review
  6. Review
  7. Review
  8. Can Activation of NRF2 Be a Strategy against COVID-19?Trends in pharmacological sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article
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

2 authors at 1 institution in 1 country.

Eun-Ryeong Hahm2.32A Hillman Cancer Center Research Pavilion, University of Pittsburgh Cancer Institute, 5117 Centre Avenue, Pittsburgh, PA 15213, USA.
Shivendra V Singh
UPMC Hillman Cancer Center · US

Funding

Anticarcinogenic Effect of ITCs Against Prostate CancerR01CA101753 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SINGH, SHIVENDRA · 2003 to 2019
$4.9M
Prevention of Prostate Cancer by SulforaphaneR01CA115498 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SINGH, SHIVENDRA · 2005 to 2015
$2.8M
NCI NIH HHS CA115498-05NCI NIH HHS R01 CA101753NCI NIH HHS R01 CA115498
6 · The paper itself

Abstract

D,L-sulforaphane (SFN), a synthetic analogue of broccoli-derived L-isomer, inhibits viability of human prostate cancer cells and prevents development of prostate cancer and distant site metastasis in a transgenic mouse model. However, the mechanism underlying the anticancer effect of SFN is not fully understood. We now show that SFN inhibits constitutive and interleukin-6 (IL-6)-inducible activation of signal transducer and activator of transcription 3 (STAT3), which is an oncogenic transcription factor activated in many human malignancies, including prostate cancer. Growth-suppressive concentrations of SFN (20 and 40 micromol/L) decreased constitutive (DU145 cells) and IL-6-induced (DU145 and LNCaP cells) phosphorylation of STAT3 (Tyr(705)) as well as its upstream regulator Janus-activated kinase 2 (Tyr(1007/1008)). Exposure of DU145 and LNCaP cells to SFN resulted in suppression of (a) IL-6-induced transcriptional activity of STAT3 as judged by luciferase reporter assay and (b) nuclear translocation of phospho-STAT3 as revealed by immunofluorescence microscopy. Levels of many STAT3-regulated gene products, including Bcl-2, cyclin D1, and survivin, were also reduced in SFN-treated cells. The IL-6-mediated activation of STAT3 conferred partial but marked protection against SFN-induced apoptosis as evidenced by cytoplasmic histone-associated DNA fragmentation and cleavage of poly(ADP-ribose) polymerase and procaspase-3. Furthermore, knockdown of STAT3 protein using small interfering RNA resulted in a modest yet statistically significant increase in SFN-induced apoptotic DNA fragmentation in DU145 cells. Suppression of STAT3 activation was also observed in cells treated with naturally occurring analogues of SFN. In conclusion, the present study indicates that inhibition of STAT3 partially contributes to the proapoptotic effect of SFN.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBrassicaceaeCell Line, TumorDNA FragmentationEnzyme ActivationGene ExpressionGene Expression RegulationHumansImmunoblottingInterleukin-6IsothiocyanatesMaleMiceMicroscopy, FluorescenceAntineoplastic AgentsInterleukin-6IsothiocyanatesPlant ExtractsSTAT3 Transcription Factor

Identifiers

PMID20233902
PMCPMC2853726
OpenAlexW2154062229

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.