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ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas

The mechanism of progression from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) remains largely unknown. We compared gene expression in tumors with simultaneous DCIS and IDC to decipher how diverse proteins participate in the local invasive process. Twenty frozen tumor specimens...

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Autores principales: Castellana, Bàrbara, Escuin, Daniel, Peiró, Gloria, Garcia-Valdecasas, Bárbara, Vázquez, Tania, Pons, Cristina, Pérez-Olabarria, Maitane, Barnadas, Agustí, Lerma, Enrique
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328783/
https://www.ncbi.nlm.nih.gov/pubmed/22514560
http://dx.doi.org/10.7150/jca.4120
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author Castellana, Bàrbara
Escuin, Daniel
Peiró, Gloria
Garcia-Valdecasas, Bárbara
Vázquez, Tania
Pons, Cristina
Pérez-Olabarria, Maitane
Barnadas, Agustí
Lerma, Enrique
author_facet Castellana, Bàrbara
Escuin, Daniel
Peiró, Gloria
Garcia-Valdecasas, Bárbara
Vázquez, Tania
Pons, Cristina
Pérez-Olabarria, Maitane
Barnadas, Agustí
Lerma, Enrique
author_sort Castellana, Bàrbara
collection PubMed
description The mechanism of progression from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) remains largely unknown. We compared gene expression in tumors with simultaneous DCIS and IDC to decipher how diverse proteins participate in the local invasive process. Twenty frozen tumor specimens with concurrent, but separated, DCIS and IDC were microdissected and evaluated. Total RNA was extracted and microarray analysis was performed using Affymetrix GeneChip® Human Gene 1.0 ST Arrays. Microarray data were validated by quantitative real time reverse transcription-PCR (qRT-PCR) and immunohistochemistry. Controls included seven pure in situ carcinomas, eight fragments from normal breast tissue, and a series of mouse breast carcinomas (MMTV-PyMT). Fifty-six genes were differentially expressed between DCIS and IDC samples. The genes upregulated in IDC samples, and probably associated with invasion, were related to the epithelial-mesenchymal transition (ASPN, THBS2, FN1, SPARC, and COL11A1), cellular adhesion (GJB2), cell motility and progression (PLAUR, PLAU, BGN, ADAMTS16, and ENPP2), extracellular matrix degradation (MMP11, MMP13, and MMP14), and growth/proliferation (ST6GAL2). qRT-PCR confirmed the expression patterns of ASPN, GJB2, ENPP2, ST6GAL2, and TMBS10. Expression of the ASPN and GJB2 gene products was detected by immunohistochemistry in invasive carcinoma foci. The association of GJB2 protein expression with invasion was confirmed by qRT-PCR in mouse tumors (P < 0.05). Conclusions: The upregulation of ASPN and GJB2 may play important roles in local invasion of breast ductal carcinomas.
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spelling pubmed-33287832012-04-18 ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas Castellana, Bàrbara Escuin, Daniel Peiró, Gloria Garcia-Valdecasas, Bárbara Vázquez, Tania Pons, Cristina Pérez-Olabarria, Maitane Barnadas, Agustí Lerma, Enrique J Cancer Research Paper The mechanism of progression from ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) remains largely unknown. We compared gene expression in tumors with simultaneous DCIS and IDC to decipher how diverse proteins participate in the local invasive process. Twenty frozen tumor specimens with concurrent, but separated, DCIS and IDC were microdissected and evaluated. Total RNA was extracted and microarray analysis was performed using Affymetrix GeneChip® Human Gene 1.0 ST Arrays. Microarray data were validated by quantitative real time reverse transcription-PCR (qRT-PCR) and immunohistochemistry. Controls included seven pure in situ carcinomas, eight fragments from normal breast tissue, and a series of mouse breast carcinomas (MMTV-PyMT). Fifty-six genes were differentially expressed between DCIS and IDC samples. The genes upregulated in IDC samples, and probably associated with invasion, were related to the epithelial-mesenchymal transition (ASPN, THBS2, FN1, SPARC, and COL11A1), cellular adhesion (GJB2), cell motility and progression (PLAUR, PLAU, BGN, ADAMTS16, and ENPP2), extracellular matrix degradation (MMP11, MMP13, and MMP14), and growth/proliferation (ST6GAL2). qRT-PCR confirmed the expression patterns of ASPN, GJB2, ENPP2, ST6GAL2, and TMBS10. Expression of the ASPN and GJB2 gene products was detected by immunohistochemistry in invasive carcinoma foci. The association of GJB2 protein expression with invasion was confirmed by qRT-PCR in mouse tumors (P < 0.05). Conclusions: The upregulation of ASPN and GJB2 may play important roles in local invasion of breast ductal carcinomas. Ivyspring International Publisher 2012-04-16 /pmc/articles/PMC3328783/ /pubmed/22514560 http://dx.doi.org/10.7150/jca.4120 Text en © Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.
spellingShingle Research Paper
Castellana, Bàrbara
Escuin, Daniel
Peiró, Gloria
Garcia-Valdecasas, Bárbara
Vázquez, Tania
Pons, Cristina
Pérez-Olabarria, Maitane
Barnadas, Agustí
Lerma, Enrique
ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title_full ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title_fullStr ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title_full_unstemmed ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title_short ASPN and GJB2 Are Implicated in the Mechanisms of Invasion of Ductal Breast Carcinomas
title_sort aspn and gjb2 are implicated in the mechanisms of invasion of ductal breast carcinomas
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328783/
https://www.ncbi.nlm.nih.gov/pubmed/22514560
http://dx.doi.org/10.7150/jca.4120
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