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Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion

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Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion. / Kreßner, Camilla; Nollau, Peter; Grosse, Robert; Brandt, Dominique T.

in: PLOS ONE, Jahrgang 8, Nr. 8, 01.01.2013, S. e69947.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kreßner, C, Nollau, P, Grosse, R & Brandt, DT 2013, 'Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion', PLOS ONE, Jg. 8, Nr. 8, S. e69947. https://doi.org/10.1371/journal.pone.0069947

APA

Kreßner, C., Nollau, P., Grosse, R., & Brandt, D. T. (2013). Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion. PLOS ONE, 8(8), e69947. https://doi.org/10.1371/journal.pone.0069947

Vancouver

Kreßner C, Nollau P, Grosse R, Brandt DT. Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion. PLOS ONE. 2013 Jan 1;8(8):e69947. https://doi.org/10.1371/journal.pone.0069947

Bibtex

@article{78b6de8e69e0474f88c3b85ab7dfed52,
title = "Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion",
abstract = "We have recently characterized SCAI (Suppressor of Cancer Cell Invasion), a transcriptional modulator regulating cancer cell motility through suppression of MAL/SRF dependent gene transcription. We show here that SCAI is expressed in a wide range of normal human tissues and its expression is diminished in a large array of primary human breast cancer samples indicating that SCAI expression might be linked to the etiology of human cancer. To establish a functional link between SCAI and tumorigenesis we performed affinity columns to identify SCAI-interacting proteins. Our data show that SCAI interacts with the tumor suppressing SWI/SNF chromatin remodeling complex to promote changes in gene expression and the invasive capacities of human tumor cells. Moreover our data implicate a functional hierarchy between SCAI and BRM, since SCAI function is abrogated in the absence of BRM expression.",
keywords = "Breast Neoplasms, Cell Movement, Cells, Cultured, Chromosomal Proteins, Non-Histone, Female, Genes, Reporter, HEK293 Cells, Humans, Immunoprecipitation, Neoplasm Invasiveness, Transcription Factors, Transcription, Genetic, Tumor Suppressor Proteins",
author = "Camilla Kre{\ss}ner and Peter Nollau and Robert Grosse and Brandt, {Dominique T}",
year = "2013",
month = jan,
day = "1",
doi = "10.1371/journal.pone.0069947",
language = "English",
volume = "8",
pages = "e69947",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "8",

}

RIS

TY - JOUR

T1 - Functional interaction of SCAI with the SWI/SNF complex for transcription and tumor cell invasion

AU - Kreßner, Camilla

AU - Nollau, Peter

AU - Grosse, Robert

AU - Brandt, Dominique T

PY - 2013/1/1

Y1 - 2013/1/1

N2 - We have recently characterized SCAI (Suppressor of Cancer Cell Invasion), a transcriptional modulator regulating cancer cell motility through suppression of MAL/SRF dependent gene transcription. We show here that SCAI is expressed in a wide range of normal human tissues and its expression is diminished in a large array of primary human breast cancer samples indicating that SCAI expression might be linked to the etiology of human cancer. To establish a functional link between SCAI and tumorigenesis we performed affinity columns to identify SCAI-interacting proteins. Our data show that SCAI interacts with the tumor suppressing SWI/SNF chromatin remodeling complex to promote changes in gene expression and the invasive capacities of human tumor cells. Moreover our data implicate a functional hierarchy between SCAI and BRM, since SCAI function is abrogated in the absence of BRM expression.

AB - We have recently characterized SCAI (Suppressor of Cancer Cell Invasion), a transcriptional modulator regulating cancer cell motility through suppression of MAL/SRF dependent gene transcription. We show here that SCAI is expressed in a wide range of normal human tissues and its expression is diminished in a large array of primary human breast cancer samples indicating that SCAI expression might be linked to the etiology of human cancer. To establish a functional link between SCAI and tumorigenesis we performed affinity columns to identify SCAI-interacting proteins. Our data show that SCAI interacts with the tumor suppressing SWI/SNF chromatin remodeling complex to promote changes in gene expression and the invasive capacities of human tumor cells. Moreover our data implicate a functional hierarchy between SCAI and BRM, since SCAI function is abrogated in the absence of BRM expression.

KW - Breast Neoplasms

KW - Cell Movement

KW - Cells, Cultured

KW - Chromosomal Proteins, Non-Histone

KW - Female

KW - Genes, Reporter

KW - HEK293 Cells

KW - Humans

KW - Immunoprecipitation

KW - Neoplasm Invasiveness

KW - Transcription Factors

KW - Transcription, Genetic

KW - Tumor Suppressor Proteins

U2 - 10.1371/journal.pone.0069947

DO - 10.1371/journal.pone.0069947

M3 - SCORING: Journal article

C2 - 23936361

VL - 8

SP - e69947

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 8

ER -