Evidence map›Paper›PMID 17982488›Full record

ArticleOncogene2008

Wild-type p53 and p73 negatively regulate expression of proliferation related genes.

M J Scian, E H Carchman, L Mohanraj, K E R Stagliano, M A E Anderson, D Deb, B M Crane, T Kiyono, B Windle, S P Deb and 1 more

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

38 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

11 authors at 1 institution in 1 country.

M J ScianDepartment of Biochemistry and Molecular Biology and the Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, USA.
E H Carchman
L Mohanraj
K E R Stagliano
M A E Anderson
D Deb
B M Crane
T Kiyono
B Windle
S P Deb
S Deb
Virginia Commonwealth University · US

Funding

OVEREXPRESSION OF MDM2 IN THE ETIOLOGY OF BREAST CANCERR01CA074172 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DEB, SWATI P · 1998 to 2001
$448k
BREAST CANCER ETIOLOGY--P53 GAIN OF FUNCTION MUTATIONSR01CA070712 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DEB, SUMITRA · 1996 to 2000
$223k
Role of Tumor Suppressor p53 in Breast CancerF31CA097520 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SCIAN, MARIANO J · 2002 to 2004
$87k
NCI NIH HHS CA70712NCI NIH HHS CA74172NCI NIH HHS F31-CA97520
6 · The paper itself

Abstract

When normal cells come under stress, the wild-type (WT) p53 level increases resulting in the regulation of gene expression responsible for growth arrest or apoptosis. Here we show that elevated levels of WT p53 or its homologue, p73, inhibit expression of a number of cell cycle regulatory and growth promoting genes. Our analysis also identified a group of genes whose expression is differentially regulated by WT p53 and p73. We have infected p53-null H1299 human lung carcinoma cells with recombinant adenoviruses expressing WT p53, p73 or beta-galactosidase, and have undertaken microarray hybridization analyses to identify genes whose expression profile is altered by p53 or p73. Quantitative real-time PCR verified the repression of E2F-5, centromere protein A and E, minichromosome maintenance proteins (MCM)-2, -3, -5, -6 and -7 and human CDC25B after p53 expression. 5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of the cyclin B2 protein level suggesting that DNA damage may indeed cause repression of these genes. Transient transcriptional assays verified that WT p53 repressed promoters of a number of these genes. Interestingly, a gain-of-function p53 mutant instead upregulated a number of these promoters in transient transfection. Using promoter deletion mutants of MCM-7 we have found that WT p53-mediated repression needs a minimal promoter that contains a single E2F site and surrounding sequences. However, a single E2F site cannot be significantly repressed by WT p53. Many of the genes identified are also repressed by p21. Thus, our work shows that WT p53 and p73 repress a number of growth-related genes and that in many instances this repression may be through the induction of p21.

Indexed as

Cell ProliferationApoptosisBase SequenceCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsDNA DamageE2F5 Transcription FactorGene Expression ProfilingGene Expression RegulationHumansNuclear ProteinsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticSequence DeletionTumor Protein p73Cell Cycle ProteinsDNA-Binding ProteinsE2F5 protein, humanE2F5 Transcription FactorNuclear ProteinsTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID17982488
OpenAlexW2074939483

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.