Evidence map›Paper›PMID 15467735›Full record

ArticleOncogene2004

HES-1 inhibits 17beta-estradiol and heregulin-beta1-mediated upregulation of E2F-1.

Johan Hartman, Patrick Müller, James S Foster, Jay Wimalasena, Jan-Ake Gustafsson, Anders Ström

Abstract read
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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 63 citations in OpenAlex.

  1. HES1 oscillations are required for cell cycle reentry in oestrogen receptor-positive breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  5. Differential phase register of Hes1 oscillations with mitoses underlies cell-cycle heterogeneity in ERProceedings of the National Academy of Sciences of the United States of America · 2021
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  9. Oncology letters · 2016
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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

6 authors at 2 institutions in 2 countries.

Johan HartmanCenter for Biotechnology, Department of BioSciences, Karolinska Institutet, Novum, S-141 57 Huddinge Sweden.
Patrick Müller
James S Foster
Jay Wimalasena
Jan-Ake Gustafsson
Anders Ström
Karolinska Institutet · SEUniversity of Tennessee Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that expression of the transcription factor HES-1 is required for the growth-inhibitory effect of all-trans retinoic acid on MCF-7 cells. In this study, we have used T47D cells with tetracyclin-regulated expression of wild-type or a dominant-negative form of HES-1. Expression of HES-1 in T47D cells inhibited G1/S-phase transition and activation of Cdk2 elicited by estrogen. Estrogen treatment of T47D cells caused increased expression of E2F-1, and this expression was inhibited by cotreatment with all-trans retinoic acid. We show that the effect is mediated through HES-1, which directly downregulates E2F-1 expression through a CACGAG-site within the E2F-1 promoter. Furthermore, proliferation caused by heregulin-beta1 treatment of T47D cells was inhibited by all-trans retinoic acid and this effect was mediated by HES-1. Interestingly, heregulin-beta1-mediated upregulation of E2F-1 expression was directly inhibited by HES-1 through the same CACGAG-site as seen with estrogen-stimulated induction. In addition, we found that two important downstream target genes of estrogen and heregulin-beta1 that are regulated through E2F-1, cyclin E and NPAT, were both regulated in a similar fashion by all-trans retinoic acid, and these effects were antagonized by dominant-negative HES-1. These findings establish that HES-1 inhibits both estrogen- and heregulin-beta1-stimulated growth of breast cancer cells, and further suggest that growth inhibition induced in these cells by all-trans retinoic acid occurs via HES-1-mediated downregulation of E2F-1 expression.

Indexed as

Base SequenceBasic Helix-Loop-Helix ProteinsBlotting, WesternCell Cycle ProteinsCell Line, TumorDNA-Binding ProteinsDNA, ComplementaryDNA PrimersE2F1 Transcription FactorE2F Transcription FactorsElectrophoretic Mobility Shift AssayEstradiolFlow CytometryHomeodomain ProteinsHumansNeuregulin-1Basic Helix-Loop-Helix ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA, ComplementaryDNA PrimersE2F1 protein, humanE2F1 Transcription FactorE2F Transcription FactorsEstradiolheregulin beta1HES1 protein, humanHomeodomain ProteinsNeuregulin-1Transcription Factor HES-1Transcription Factors

Identifiers

PMID15467735
OpenAlexW2032794576

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.