Evidence map›Paper›PMID 23169992›Full record

ArticleThe Journal of endocrinology2013

SIRT1 represses estrogen-signaling, ligand-independent ERα-mediated transcription, and cell proliferation in estrogen-responsive breast cells.

Robert L Moore, Douglas V Faller

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
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  19. Review
  20. SIRT1 induces tumor invasion by targeting epithelial mesenchymal transition-related pathway and is a prognostic marker in triple negative breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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.

Robert L MooreCancer Center, Boston University School of Medicine, 72 East Concord Street, Room K-701, Boston, Massachusetts 02118-2307, USA.
Douglas V Faller
Boston University · US

Funding

Signal Transduction by Androgen in Prostate CellsR01CA101992 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI FALLER, DOUGLAS V · 2004 to 2013
$2.4M
NCI NIH HHS CA101992S1NCI NIH HHS R01 CA101992NCI NIH HHS R01-CA101992
6 · The paper itself

Abstract

In prostate and breast cancer, the androgen receptor and estrogen receptor (ER) mediate induction of androgen- and estrogen-responsive genes respectively and stimulate cell proliferation in response to the binding of their cognate steroid hormones. Sirtuin 1 (SIRT1) is a NAD+-dependent class III histone deacetylase that has been linked to gene silencing, control of the cell cycle, apoptosis, and energy homeostasis. In prostate cancer, SIRT1 is required for androgen antagonist-mediated transcriptional repression and growth suppression of prostate cancer cells. Whether SIRT1 plays a similar role in the actions of estrogen or antagonists had not been determined. We report here that SIRT1 represses the transcriptional and proliferative response of breast cancer cells to estrogens, and this repression is ERα dependent. Inhibition of SIRT1 activity results in the phosphorylation of ERα in an AKT-dependent manner, and this activation requires phosphoinositide 3-kinase activity. Phosphorylated ERα subsequently accumulates in the nucleus, where ERα binds DNA ER-responsive elements and activates transcription of estrogen-responsive genes. This ER-dependent transcriptional activation augments estrogen-induced signaling, but also activates ER signaling in the absence of estrogen, thus defining a novel and unexpected mechanism of ligand-independent ERα-mediated activation and target gene transcription. Like ligand-dependent activation of ERα, SIRT1 inhibition-mediated ERα activation in the absence of estrogen also results in breast cancer cell proliferation. Together, these data demonstrate that SIRT1 regulates the most important cell signaling pathway for the growth of breast cancer cells, both in the presence and the absence of estrogen.

Indexed as

BenzamidesCell Line, TumorCell ProliferationEstrogen Receptor alphaEstrogensGene Expression Regulation, NeoplasticHumansNaphtholsPhosphorylationPromoter Regions, GeneticProto-Oncogene Proteins c-aktSignal TransductionSirtuin 1Transcription, GeneticBenzamidesEstrogen Receptor alphaEstrogensNaphtholsProto-Oncogene Proteins c-aktSIRT1 protein, humansirtinolSirtuin 1

Identifiers

PMID23169992
PMCPMC3852670
OpenAlexW2163137479

What OpenQuestion holds

Textmetadata
LicenceTDM
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.