Evidence map›Paper›PMID 17637753›Full record

ArticleOncogene2008

The AP-1 transcription factor regulates breast cancer cell growth via cyclins and E2F factors.

Q Shen, I P Uray, Y Li, T I Krisko, T E Strecker, H-T Kim, P H Brown

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
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  3. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
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  9. Cell growth and the cell cycle: New insights about persistent questions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Review
  10. Article
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

11 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

7 authors at 1 institution in 1 country.

Q ShenBreast Center, Departments of Medicine and Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
I P Uray
Y Li
T I Krisko
T E Strecker
H-T Kim
P H Brown
Baylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activating protein-1 (AP-1) transcription factor transduces growth signals through signal transduction pathways to the nucleus, leading to the expression of genes involved in growth and malignant transformation in many cell types. We have previously shown that overexpression of a dominant negative form of the cJun proto-oncogene, a cJun dominant negative mutant (Tam67), blocks AP-1 transcriptional activity, induces a G(1) cell cycle block and inhibits breast cancer cell growth in vitro and in vivo. We found that AP-1 blockade by Tam67 in MCF-7 breast cancer cells downregulates cyclin D1 transcriptional activity by at least two mechanisms: by suppressing transcription at the known AP-1 binding site (-934/-928) and by suppressing growth factor-induced expression through suppressing E2F activation at the E2F-responsive site (-726/-719). AP-1 blockade also led to reduced expression of E2F1 and E2F2, but not E2F4, at the mRNA and protein levels. Chromatin immunoprecipitation and supershift assays demonstrated that AP-1 blockade caused decreased binding of E2F1 protein to the E2F site in the cyclin D1 promoter. We also found that Tam67 suppressed the expression of the E2F1 dimerizing partner, DP1 and E2F-upregulated cell cycle genes (cyclins E, A, B and D3) and enhanced the expression of E2F-downregulated cell cycle genes (cyclins G(2) and I). Reduced expression of other E2F-regulated genes was also seen with AP-1 blockade and E2F suppression. Thus, the AP-1 factor regulates the expression of cyclin D and E2F (the latter in turn regulates E2F-downstream genes), leading to cell cycle progression and breast cancer cell proliferation.

Indexed as

Breast NeoplasmsCell Line, TumorCell ProliferationChromatin ImmunoprecipitationCyclin D1CyclinsDown-RegulationE2F1 Transcription FactorE2F2 Transcription FactorE2F4 Transcription FactorE2F Transcription FactorsFemaleGene Expression Regulation, NeoplasticHumansPeptide FragmentsPromoter Regions, GeneticCyclin D1CyclinsE2F1 protein, humanE2F1 Transcription FactorE2F2 Transcription FactorE2F4 Transcription FactorE2F Transcription FactorsMAS1 protein, humanPeptide FragmentsProto-Oncogene MasProto-Oncogene Proteins c-junRNA, MessengerTAM67 peptideTranscription Factor AP-1Transcription Factor DP1

Identifiers

PMID17637753
OpenAlexW2153733894

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.