Evidence map›Paper›PMID 18211900›Full record

ArticleThe Journal of biological chemistry2008

Alterations of BRMS1-ARID4A interaction modify gene expression but still suppress metastasis in human breast cancer cells.

Douglas R Hurst, Yi Xie, Kedar S Vaidya, Alka Mehta, Blake P Moore, Mary Ann Accavitti-Loper, Rajeev S Samant, Ritu Saxena, Alexandra C Silveira, Danny R Welch

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Noncoding RNAs, Vital Players in Breast Cancer Metastasis.Breast cancer (Dove Medical Press) · 2025
    Review
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  18. Structural insights into the assembly of the histone deacetylase-associated Sin3L/Rpd3L corepressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Douglas R HurstDepartment of Pathology, University of Alabama, Birmingham, Alabama 35294, USA.
Yi Xie
Kedar S Vaidya
Alka Mehta
Blake P Moore
Mary Ann Accavitti-Loper
Rajeev S Samant
Ritu Saxena
Alexandra C Silveira
Danny R Welch
University of Alabama at Birmingham · USUSA Mitchell Cancer Institute · US

Funding

MOLECULAR REGULATION OF BREAST CANCER METASTASISR01CA087728 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WELCH, DANNY R. · 2000 to 2008
$2.7M
Mechanistic Insight into BRMS1 Suppression of MetastasisF32CA113037 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HURST, DOUGLAS R · 2005 to 2007
$143k
NCI NIH HHS CA87728NCI NIH HHS F32 CA113037NCI NIH HHS F32CA113037NCI NIH HHS R01 CA087728
6 · The paper itself

Abstract

The BRMS1 metastasis suppressor interacts with the protein AT-rich interactive domain 4A (ARID4A, RBBP1) as part of SIN3.histone deacetylase chromatin remodeling complexes. These transcriptional co-repressors regulate diverse cell phenotypes depending upon complex composition. To define BRMS1 complexes and their roles in metastasis suppression, we generated BRMS1 mutants (BRMS1(mut)) and mapped ARID4A interactions. BRMS1(L174D) disrupted direct interaction with ARID4A in yeast two-hybrid genetic screens but retained an indirect association with ARID4A in MDA-MB-231 and -435 human breast cancer cell lines by co-immunoprecipitation. Deletion of the first coiled-coil domain (BRMS1(DeltaCC1)) did not disrupt direct interaction in yeast two-hybrid screens but did prevent association by co-immunoprecipitation. These results suggest altered complex composition with BRMS1(mut). Although basal transcription repression was impaired and the pro-metastatic protein osteopontin was differentially down-regulated by BRMS1(L174D) and BRMS1(DeltaCC1), both down-regulated the epidermal growth factor receptor and suppressed metastasis in MDA-MB-231 and -435 breast cancer xenograft models. We conclude that BRMS1(mut), which modifies the composition of a SIN3.histone deacetylase chromatin remodeling complex, leads to altered gene expression profiles. Because metastasis requires the coordinate expression of multiple genes, down-regulation of at least one important gene, such as the epidermal growth factor receptor, had the ability to suppress metastasis. Understanding which interactions are necessary for particular biochemical/cellular functions may prove important for future strategies targeting metastasis.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorDown-RegulationErbB ReceptorsFemaleHistone DeacetylasesHumansMiceMutationNeoplasm MetastasisNeoplasm ProteinsNeoplasm TransplantationArid4a protein, mouseBRMS1 protein, humanCarrier ProteinsEGFR protein, humanErbB ReceptorsHistone DeacetylasesNeoplasm ProteinsOsteopontinRepressor ProteinsRetinoblastoma-Binding Protein 1Sin3 Histone Deacetylase and Corepressor Complex

Identifiers

PMID18211900
PMCPMC2293288
OpenAlexW1987728370

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.