Evidence map›Paper›PMID 15064752›Full record

ArticleOncogene2004

Dominant-negative c-Jun (TAM67) target genes: HMGA1 is required for tumor promoter-induced transformation.

Arindam Dhar, Jing Hu, Raymond Reeves, Linda M S Resar, Nancy H Colburn

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. FRA-1 as a Regulator of EMT and Metastasis in Breast Cancer.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Hitting the bull's eye: targeting HMGA1 in cancer stem cells.Expert review of anticancer therapy · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. 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 3 institutions in 1 country.

Arindam DharGene Regulation Section, Laboratory of Cancer Prevention, NCI at Frederick, Frederick, MD 21702-1201, USA. adhar@ncifcrf.gov
Jing Hu
Raymond Reeves
Linda M S Resar
Nancy H Colburn
Frederick National Laboratory for Cancer Research · USJohns Hopkins University · USWashington State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the transcription factor AP-1 (activator protein-1) is required for tumor promotion and maintenance of malignant phenotype. A number of AP-1-regulated genes that play a role in tumor progression have been identified. However, AP-1-regulated genes driving tumor induction are yet to be defined. Previous studies have established that expression of a dominant-negative c-Jun (TAM67) inhibits phorbol 12-tetradecanoyl-13-acetate (TPA)-induced AP-1 transactivation as well as transformation in mouse epidermal JB6/P+ cells and tumor promotion in mouse skin carcinogenesis. In this study, we utilized the tumor promotion-sensitive JB6/P+ cells to identify AP-1-regulated TAM67 target genes and to establish causal significance in transformation for one target gene. A 2700 cDNA microarray was queried with RNA from TPA-treated P+ cells with or without TAM67 expression. Under conditions in which TAM expression inhibited TPA-induced transformation, microarray analysis identified a subset of six genes induced by TPA and suppressed by TAM67. One of the identified genes, the high-mobility group protein A1 (Hmga1) is induced by TPA in P+, but not in transformation-resistant P cells. We show that TPA induction of the architectural transcription factor HMGA1 is inhibited by TAM67, is extracellular-signal-regulated kinase (ERK)-activation dependent, and is mediated by AP-1. HMGA1 antisense construct transfected into P+ cells blocked HMGA1 protein expression and inhibited TPA-induced transformation indicating that HMGA1 is required for transformation. HMGA1 is not however sufficient as HMGA1a or HMGA1b overexpression did not confer transformation sensitivity on P- cells. Although HMGA1 expression is ERK dependent, it is not the only ERK-dependent event required for transformation because it does not suffice to rescue ERK-deficient P- cells. Our study shows (a) TAM 67 when it inhibits AP-1 and transformation, targets a relatively small number of genes; (b) HMGA1, a TAM67 target gene, is causally related to transformation and therefore a potentially important target for cancer prevention.

Indexed as

Epidermal CellsMAP Kinase Kinase Kinase 1AnimalsButadienesCell LineCell Transformation, NeoplasticClone CellsCyclin D1Disease SusceptibilityDNA, ComplementaryEpidermisGene Expression ProfilingGenes, junHMGA1a ProteinHMGA1b ProteinMAP Kinase Kinase KinasesButadienesCyclin D1DNA, ComplementaryHMGA1a ProteinHMGA1b ProteinMap3k1 protein, mouseMAP Kinase Kinase Kinase 1MAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesNitrilesOligonucleotides, AntisenseOsteopontinProto-Oncogene Proteins c-junSialoglycoproteinsSpp1 protein, mouseTetradecanoylphorbol AcetateTranscription Factor AP-1U 0126

Identifiers

PMID15064752
OpenAlexW1965467838

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.