Evidence map›Paper›PMID 9888461›Full record

ArticleBritish journal of cancer1999

Transcriptional repression of the human collagenase-1 (MMP-1) gene in MDA231 breast cancer cells by all-trans-retinoic acid requires distal regions of the promoter.

U Benbow, J L Rutter, C H Lowrey, C E Brinckerhoff

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. No association between matrix metalloproteinase-1 or matrix metalloproteinase-3 polymorphisms and breast cancer susceptibility: a report from the Shanghai Breast Cancer Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2009
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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

4 authors at 1 institution in 1 country.

U BenbowDepartment of Medicine, Dartmouth Medical School, Hanover NH 03755, USA.
J L Rutter
C H Lowrey
C E Brinckerhoff
Dartmouth College · US

Funding

Cancer Biology and Molecular TherapeuticsT32CA009658 · NCI · DARTMOUTH COLLEGE · PI EASTMAN, ALAN R · 1991 to 2011
$3.8M
REGULATION OF BETA-GLOBIN LOCUS CHROMATIN STRUCTURER01HL052243 · NHLBI · DARTMOUTH COLLEGE · PI LOWREY, CHRISTOPHER H. · 1995 to 2006
$2.2M
REGULATION OF COLLAGENASE GENE EXPRESSIONR37AR026599 · NIAMS · DARTMOUTH COLLEGE · PI BRINCKERHOFF, CONSTANCE E · 1999 to 2006
$1.9M
REGULATION OF METALLOPROTEINASE GENE EXPRESSIONR01AR026599 · NIAMS · DARTMOUTH COLLEGE · PI BRINCKERHOFF, CONSTANCE E · 1986 to 2011
$1.7M
NCI NIH HHS T32-CA-09658NHLBI NIH HHS HL-52243NIAMS NIH HHS AR-26599
6 · The paper itself

Abstract

In the present study, we investigated the mechanisms controlling constitutive transcription of collagenase-1 and its repression by all-trans-retinoic acid (RA) in the highly invasive metastatic and oestrogen-receptor-negative breast cancer cell line MDA231. A combination of in vivo and in vitro experiments that include DNAase I hypersensitivity assays, transient transfection of collagenase-1 promoter constructs, and electrophoretic mobility shift assays implicate several PEA3 sites, binding sites for Ets-related transcription factors, in the constitutive expression of the human collagenase-1 promoter. Transient transfection of promoter constructs linked to the luciferase reporter, along with gel retardation assays, revealed that repression of collagenase-1 transcription by RA is not dependent on the proximal AP-1 site, but, rather, requires sequences located in distal regions of the promoter. Transcriptional analyses and electrophoretic mobility shift assays suggest that the PEA3 site located at -3108 bp facilitates, at least in part, the transcriptional repression of the human collagenase-1 gene in MDA231 cells. We conclude that collagenase-1 repression in MDA231 cells occurs by a novel regulatory pathway that does not depend on the proximal AP-1 site at -73 bp, but does depend on distal regions in the collagenase-1 promoter.

Indexed as

CollagenasesDeoxyribonuclease IEnzyme RepressionFemaleGene ExpressionHumansMatrix Metalloproteinase 1Matrix Metalloproteinase InhibitorsNeoplasm ProteinsPromoter Regions, GeneticReceptors, Retinoic AcidRetinoic Acid Receptor alphaRetinoic Acid Receptor gammaTranscription, GeneticTransfectionTretinoinCollagenasesDeoxyribonuclease IMatrix Metalloproteinase 1Matrix Metalloproteinase InhibitorsNeoplasm ProteinsRARA protein, humanReceptors, Retinoic AcidRetinoic Acid Receptor alpharetinoic acid receptor betaRetinoic Acid Receptor gammaTretinoin

Identifiers

PMID9888461
PMCPMC2362185
OpenAlexW2079582132

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.