Evidence map›Paper›PMID 16617102›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

MTA1, a transcriptional activator of breast cancer amplified sequence 3.

Anupama E Gururaj, Rajesh R Singh, Suresh K Rayala, Caroline Holm, Petra den Hollander, Hao Zhang, Seetharaman Balasenthil, Amjad H Talukder, Goran Landberg, Rakesh Kumar

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  16. Frontiers in pharmacology · 2017
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  17. Review
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  20. MTA1 promotes metastasis of MPM via suppression of E-cadherin.Journal of experimental & clinical cancer research : CR · 2015
    Article

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Anupama E GururajDepartment of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.
Rajesh R Singh
Suresh K Rayala
Caroline Holm
Petra den Hollander
Hao Zhang
Seetharaman Balasenthil
Amjad H Talukder
Goran Landberg
Rakesh Kumar
The University of Texas MD Anderson Cancer Center · USLund University · SE

Funding

Role of Metastatic Tumor Antigen-1 in Mammary GlandR01CA098823 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KUMAR, RAKESH · 2003 to 2013
$3.1M
RECEPTOR BLOCKADE FOR BREAST CANCERR01CA065746 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KUMAR, RAKESH · 1999 to 2007
$1.9M
SERM Regulation of PAK Pathway in Endometrial CancerR01CA109379 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KUMAR, RAKESH · 2004 to 2008
$1.5M
LABORATORY STUDY OF CHEMOTHERAPY PLUS RECEPTOR BLOCKADEU01CA065746 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI MENDELSOHN, JOHN · 1995 to 1998
–
NCI NIH HHS CA098823NCI NIH HHS CA109379NCI NIH HHS CA65746NCI NIH HHS R01 CA065746NCI NIH HHS R01 CA098823NCI NIH HHS R01 CA109379NCI NIH HHS U01 CA065746
6 · The paper itself

Abstract

Here we define a function of metastasis-associated protein 1 (MTA1), a presumed corepressor of estrogen receptor alpha (ERalpha), as a transcriptional activator of Breast Cancer Amplified Sequence 3 (BCAS3), a gene amplified and overexpressed in breast cancers. We identified BCAS3 as a MTA1 chromatin target in a functional genomic screen. MTA1 stimulation of BCAS3 transcription required ERalpha and involved a functional ERE half-site in BCAS3. Furthermore, we discovered that MTA1 is acetylated on lysine 626, and that this acetylation is necessary for a productive transcriptional recruitment of RNA polymerase II complex to the BCAS3 enhancer sequence. BCAS3 expression was elevated in mammary tumors from MTA1 transgenic mice and 60% of the human breast tumors, and correlated with the coexpression of MTA1 as well as with tumor grade and proliferation of primary breast tumor samples. These findings reveal a previously unrecognized function of MTA1 in stimulating BCAS3 expression and suggest an important role for MTA1-BCAS3 pathway in promoting cancerous phenotypes in breast tumor cells.

Indexed as

AcetylationAmino Acid SequenceBase SequenceBinding SitesBreast NeoplasmsCell Line, TumorDNA, NeoplasmEnhancer Elements, GeneticEstradiolEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHistone DeacetylasesHumansMolecular Sequence DataNeoplasm ProteinsBCAS3 protein, humanDNA, NeoplasmEstradiolEstrogen Receptor alphaHistone DeacetylasesMTA1 protein, humanNeoplasm ProteinsRepressor ProteinsTrans-Activators

Identifiers

PMID16617102
PMCPMC1458939
OpenAlexW2104104416

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.