Evidence map›Paper›PMID 10918598›Full record

ArticleOncogene2000

Cooperation between AP1 and PEA3 sites within the progression elevated gene-3 (PEG-3) promoter regulate basal and differential expression of PEG-3 during progression of the oncogenic phenotype in transformed rat embryo cells.

Z Su, Y Shi, P B Fisher

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 44 citations in OpenAlex.

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  15. Dual cancer-specific targeting strategy cures primary and distant breast carcinomas in nude mice.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  16. Targeting gene expression selectively in cancer cells by using the progression-elevated gene-3 promoter.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  17. 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

3 authors at 1 institution in 1 country.

Z SuDepartment of Pathology, Herbert Irving Comprehensive Cancer Center, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.
Y Shi
P B Fisher
Columbia University · US

Funding

PROGRESSION OF THE TRANSFORMED PHENOTYPER01CA035675 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 1985 to 2007
$1.9M
NOVEL PROSTATE CANCER GENE AND MONOCLONAL ANTIBODYR01CA074468 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FISHER, PAUL B · 1998 to 2002
$1.4M
NCI NIH HHS CA35675NCI NIH HHS CA74468
6 · The paper itself

Abstract

Cancer is a progressive disease in which a tumor cell temporally develops qualitatively new transformation related phenotypes or a further elaboration of existing transformation associated properties. Subtraction hybridization identified a novel gene associated with transformation progression in mutant adenovirus type 5, H5ts125, transformed rat embryo cells, progression elevated gene-3 (PEG-3). To define the mechanism by which expression of PEG-3 is enhanced as a function of cancer progression a 5'-flanking promoter region of approximately 2.0-kb, PEG-Prom, was isolated, cloned and characterized. The full-length and various mutated regions of the PEG-Prom were linked to a luciferase reporter construct and evaluated for promoter activity during cancer progression. These assays demonstrate a requirement for AP1 and PEA3 sites adjacent to the TATA box region of PEG-3 in mediating basal promoter activity and the enhanced expression of PEG-3 in progressed H5ts125-transformed rat embryo cells. An involvement of AP1 and PEA3 in PEG-3 regulation was also confirmed by electrophoretic mobility shift assays (EMSA) and transfection studies with cJun and PEA3 expression vectors. Our findings document the importance of both AP1 and PEA3 transcription factors in mediating basal and elevated expression of PEG-3 in H5ts125-transformed rat embryo cells displaying an aggressive and progressed cancer phenotype.

Indexed as

Antigens, DifferentiationGene Expression Regulation, NeoplasticPromoter Regions, GeneticAnimalsBase SequenceBinding SitesCell Line, TransformedCell NucleusCell Transformation, NeoplasticDNA, ComplementaryMiceMolecular Sequence DataNeoplasm ProteinsPhenotypeProtein Phosphatase 1Proto-Oncogene ProteinsAntigens, DifferentiationDNA, ComplementaryNeoplasm ProteinsPpp1r15a protein, mousePpp1r15a protein, ratProtein Phosphatase 1Proto-Oncogene ProteinsTranscription Factor AP-1transcription factor PEA3Transcription Factors

Identifiers

PMID10918598
OpenAlexW2329048545

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.