Evidence map›Paper›PMID 21737614›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Resveratrol, through NF-Y/p53/Sin3/HDAC1 complex phosphorylation, inhibits estrogen receptor alpha gene expression via p38MAPK/CK2 signaling in human breast cancer cells.

Francesca De Amicis, Francesca Giordano, Adele Vivacqua, Michele Pellegrino, Maria Luisa Panno, Donatella Tramontano, Suzanne A W Fuqua, Sebastiano Andò

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. 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
4.4field-weighted citation impact, top 6% 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, 77 citations in OpenAlex.

  1. Review
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  11. Resveratrol as Chemosensitizer Agent: State of Art and Future Perspectives.International journal of molecular sciences · 2021
    Review
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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

8 authors at 3 institutions in 2 countries.

Francesca De AmicisCentro Sanitario, Department of Pharmaco-Biology, University of Calabria, Arcavacata di Rende (CS) 87030, Italy.
Francesca Giordano
Adele Vivacqua
Michele Pellegrino
Maria Luisa Panno
Donatella Tramontano
Suzanne A W Fuqua
Sebastiano Andò
University of Calabria · ITBaylor College of Medicine · USUniversity of Naples Federico II · IT

Funding

Replication Stress and DNA Damage Response Drives ESR1 Mutant MetastasisR01CA072038 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI Suzanne AW Fuqua · 1996 to 2026
$6.7M
NCI NIH HHS R01 CA072038NCI NIH HHS R01 CA72038
6 · The paper itself

Abstract

Agents to counteract acquired resistance to hormonal therapy for breast cancer would substantially enhance the long-term benefits of hormonal therapy. In the present study, we demonstrate how resveratrol (Res) inhibits human breast cancer cell proliferation, including MCF-7 tamoxifen-resistant cells (IC(50) values for viability were in the 30-45 μM range). We show that Res, through p38(MAPK) phosphorylation, causes induction of p53, which recruits at the estrogen receptor α (ERα) proximal promoter, leading to an inhibition of ERα expression in terms of mRNA and protein content. These events appear specifically p53 dependent, since they are drastically abrogated with p53-targeting siRNA. Coimmunoprecipitation assay showed specific interaction between p53, the Sin3A corepressor, and histone deacetylase 1 (HDAC1), which was phosphorylated. The enhancement of the tripartite complex p53/Sin3A/HDAC1, together with NF-Y on Res treatment, was confirmed by chromatin immunoprecipitation analyses, with a concomitant release of Sp1 and RNA polymerase II, thereby inhibiting the cell transcriptional machinery. The persistence of such effects in MCF-7 tamoxifen-resistant cells at a higher extent than parental MCF-7 cells addresses how Res may be considered a useful pharmacological tool to be exploited in the adjuvant settings for treatment of breast cancer developing hormonal resistance.

Indexed as

Antineoplastic Agents, PhytogenicBreast NeoplasmsCasein Kinase IICCAAT-Binding FactorCell Line, TumorEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHistone Deacetylase 1Humansp38 Mitogen-Activated Protein KinasesResveratrolSin3 Histone Deacetylase and Corepressor ComplexStilbenesTumor Suppressor Protein p53Antineoplastic Agents, PhytogenicCasein Kinase IICCAAT-Binding FactorEstrogen Receptor alphaHDAC1 protein, humanHistone Deacetylase 1p38 Mitogen-Activated Protein KinasesResveratrolSin3 Histone Deacetylase and Corepressor ComplexStilbenesTumor Suppressor Protein p53

Identifiers

PMID21737614
PMCPMC3177579
OpenAlexW2012170303

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.