Evidence map›Paper›PMID 20196847›Full record

ArticleMolecular cancer2010

Sulforaphane induces cell cycle arrest by protecting RB-E2F-1 complex in epithelial ovarian cancer cells.

Christopher S Bryant, Sanjeev Kumar, Sreedhar Chamala, Jay Shah, Jagannath Pal, Mahdi Haider, Shelly Seward, Aamer M Qazi, Robert Morris, Assaad Semaan and 6 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Review
  14. Article
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  18. Article
  19. Chemopreventive activity of sulforaphane.Drug design, development and therapy · 2018
    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

16 authors at 2 institutions in 1 country.

Christopher S BryantDepartment of Surgery, Wayne State University, 4100 John R Street, Detroit, MI 48201, USA.
Sanjeev Kumar
Sreedhar Chamala
Jay Shah
Jagannath Pal
Mahdi Haider
Shelly Seward
Aamer M Qazi
Robert Morris
Assaad Semaan
Masood A Shammas
Christopher Steffes
Ravindra B Potti
Madhu Prasad
Donald W Weaver
Ramesh B Batchu
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

Telomerase And Homologous Recombination As Targets In Barrett's AdenocarcinomaR01CA125711 · NCI · WAYNE STATE UNIVERSITY · PI SHAMMAS, MASOOD A · 2008 to 2012
$1.7M
NCI NIH HHS R01 CA125711
6 · The paper itself

Abstract

backgroundSulforaphane (SFN), an isothiocyanate phytochemical present predominantly in cruciferous vegetables such as brussels sprout and broccoli, is considered a promising chemo-preventive agent against cancer. In-vitro exposure to SFN appears to result in the induction of apoptosis and cell-cycle arrest in a variety of tumor types. However, the molecular mechanisms leading to the inhibition of cell cycle progression by SFN are poorly understood in epithelial ovarian cancer cells (EOC). The aim of this study is to understand the signaling mechanisms through which SFN influences the cell growth and proliferation in EOC.

resultsSFN at concentrations of 5-20 microM induced a dose-dependent suppression of growth in cell lines MDAH 2774 and SkOV-3 with an IC50 of ~8 microM after a 3 day exposure. Combination treatment with chemotherapeutic agent, paclitaxel, resulted in additive growth suppression. SFN at ~8 microM decreased growth by 40% and 20% on day 1 in MDAH 2774 and SkOV-3, respectively. Cells treated with cytotoxic concentrations of SFN have reduced cell migration and increased apoptotic cell death via an increase in Bak/Bcl-2 ratio and cleavage of procaspase-9 and poly (ADP-ribose)-polymerase (PARP). Gene expression profile analysis of cell cycle regulated proteins demonstrated increased levels of tumor suppressor retinoblastoma protein (RB) and decreased levels of E2F-1 transcription factor. SFN treatment resulted in G1 cell cycle arrest through down modulation of RB phosphorylation and by protecting the RB-E2F-1 complex.

conclusionsSFN induces growth arrest and apoptosis in EOC cells. Inhibition of retinoblastoma (RB) phosphorylation and reduction in levels of free E2F-1 appear to play an important role in EOC growth arrest.

Indexed as

ApoptosisCell CycleCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDNA, NeoplasmE2F1 Transcription FactorEpithelial CellsFemaleGene Expression Regulation, NeoplasticHumansIsothiocyanatesNeoplasm InvasivenessOligonucleotide Array Sequence AnalysisOvarian NeoplasmsCell Cycle ProteinsDNA, NeoplasmE2F1 Transcription FactorIsothiocyanatesPaclitaxelRetinoblastoma ProteinsulforaphaneSulfoxidesThiocyanates

Identifiers

PMID20196847
PMCPMC2838815
OpenAlexW2149651943

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.