Evidence map›Paper›PMID 22427654›Full record

ArticleThe Journal of biological chemistry2012

Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent.

Yap Ching Chew, Gautam Adhikary, Gerald M Wilson, Wen Xu, Richard L Eckert

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. ACTL6A suppresses p21Oncogenesis · 2021
    Article
  9. ACTL6A suppresses p21Oncogene · 2020
    Article
  10. Article
  11. Article
  12. FABP3 in the Anterior Cingulate Cortex Modulates the Methylation Status of the Glutamic Acid DecarboxylaseThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    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

5 authors at 1 institution in 1 country.

Yap Ching ChewDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Gautam Adhikary
Gerald M Wilson
Wen Xu
Richard L Eckert
University of Maryland, Baltimore · US

Funding

MAP KINASES REGULATE INVOLUCRIN GENE EXPRESSIONR01AR046494 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI ECKERT, RICHARD L. · 2000 to 2010
$1.9M
NIAMS NIH HHS R01 AR046494
6 · The paper itself

Abstract

Sulforaphane (SFN) is an important cancer preventive agent derived from cruciferous vegetables. We show that SFN treatment suppresses normal human keratinocyte proliferation via a mechanism that involves increased expression of p21(Cip1). SFN treatment produces a concentration-dependent increase in p21(Cip1) promoter activity via a mechanism that involves stabilization of the p53 protein leading to increased p53 binding to the p21(Cip1) promoter p53 response elements. The proximal p21(Cip1) promoter GC-rich Sp1 factor binding elements are also required, as the SFN-dependent increase is lost when these sites are mutated. SFN treatment increases Sp1 binding to these elements, and the response is enhanced in the presence of exogenous Sp1 and reduced in the presence of ΔN-Sp3. CpG island methylation alters p21(Cip1) promoter activity some systems; however, expression in SFN-treated keratinocytes does not involve changes in proximal promoter methylation. The promoter is minimally methylated, and the methylation level is not altered by SFN treatment. This study indicates that SFN increases p21(Cip1) promoter transcription via a mechanism that involves SFN-dependent stabilization of p53 and increased p53 and Sp1 binding to their respective response elements in the p21(Cip1) promoter. These results are in marked contrast to the mechanisms observed in skin cancer cell lines and suggest that SFN may protect normal keratinocytes from damage while causing cancer cells to undergo apoptosis.

Indexed as

Anticarcinogenic AgentsApoptosisCell Line, TumorCpG IslandsCyclin-Dependent Kinase Inhibitor p21DNA MethylationGene Expression RegulationHumansIsothiocyanatesKeratinocytesProtein StabilityResponse ElementsSp1 Transcription FactorSulfoxidesThiocyanatesTranscription, GeneticAnticarcinogenic AgentsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21IsothiocyanatesSp1 Transcription FactorsulforaphaneSulfoxidesThiocyanatesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22427654
PMCPMC3351300
OpenAlexW2026919551

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.