Evidence map›Paper›PMID 11114728›Full record

ArticleOncogene2000

Altered Ets transcription factor activity in prostate tumor cells inhibits anchorage-independent growth, survival, and invasiveness.

G Foos, C A Hauser

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

G FoosLa Jolla Cancer Research Center, The Burnham Institute, California 92037, USA.
C A Hauser
Cancer Research Center · US

Funding

ETS TRANSCRIPTION FACTORS IN DEVELOPMENT AND CANCERR01CA074547 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI OSHIMA, ROBERT GLEN · 1997 to 2004
$2.1M
RAS INDUCED GENE EXPRESSION AND MALIGNANT TRANSFORMATIONR01CA063130 · NCI · BURNHAM INSTITUTE FOR MEDICAL RESEARCH · PI HAUSER, CRAIG A · 1995 to 2002
$958k
NCI NIH HHS CA63130NCI NIH HHS CA74547
6 · The paper itself

Abstract

The Ets family of transcription factors are important downstream targets in cellular transformation, as altering Ets activity has been found to reverse the transformed phenotype of Ras transformed mouse fibroblasts and of several human tumor cell lines. To determine whether Ets factors are important targets in the largely uncharacterized aberrant signaling in prostate cancer, we have altered Ets activity in the prostate tumor cell line PPC-1, by stable expression of either full-length Ets2, or a dominant inhibitor of Ets activity, the Ets2 DNA binding domain (Ets2DBD). Analysis of multiple independent clonal cell lines revealed that expression of either Ets2 or the Ets2DBD inhibited the anchorage-independent growth of PPC-1 cells up to 20-fold. In contrast to our previous findings with Ras-transformed NIH3T3 cells, PPC-1 cell lines expressing either Ets2 or the EtsDBD exhibited slower attached cell growth, increased Ets-dependent gene expression, and up to a 10-fold increase in apoptotic cell death. The p21cip gene was identified as a potential target of altered Ets signaling. Interestingly, the two distinct Ets2 constructs had strikingly different effects on in vitro invasiveness. Expression of the Ets2DBD almost completely blocked PPC-1 cell invasion through Matrigel, whereas over-expression of full-length Ets2 did not inhibit invasion. Overall, these results demonstrate that the balance of Ets factor activity can regulate multiple aspects of the transformed phenotype of PPC-1 prostate tumor cells, including anchorage-independent growth, survival, and invasiveness.

Indexed as

Cell Cycle ProteinsCell Transformation, NeoplasticDNA-Binding ProteinsRepressor ProteinsTranscription FactorsTumor Suppressor Proteins3T3 CellsAnimalsApoptosisBinding SitesBreast NeoplasmsCell AdhesionCell DivisionCell MovementCell SurvivalCyclin-Dependent Kinase Inhibitor p21CDKN1A protein, humanCdkn1a protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27CyclinsDNA-Binding ProteinsERF protein, humanETS2 protein, humanEts2 protein, mouseMicrotubule-Associated ProteinsPeptide FragmentsProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsRepressor ProteinsTrans-ActivatorsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID11114728
OpenAlexW2320752200

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.