A functional and regulatory network associated with PIP expression in human breast cancer.

<h4>Background</h4>The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted co...

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Autores principales: Marie-Anne Debily, Sandrine El Marhomy, Virginie Boulanger, Eric Eveno, Régine Mariage-Samson, Alessandra Camarca, Charles Auffray, Dominique Piatier-Tonneau, Sandrine Imbeaud
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Publicado: Public Library of Science (PLoS) 2009
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spelling oai:doaj.org-article:49cd927f14db420e84bfb7dc6d834b962021-11-25T06:16:55ZA functional and regulatory network associated with PIP expression in human breast cancer.1932-620310.1371/journal.pone.0004696https://doaj.org/article/49cd927f14db420e84bfb7dc6d834b962009-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19262752/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted combined gene expression profiling and network analysis studies on selected breast cancer cell lines presenting distinct PIP expression levels and hormonal receptor status, to explore the functional and regulatory network of PIP co-modulated genes.<h4>Principal findings</h4>Microarray analysis allowed identification of genes co-modulated with PIP independently of modulations resulting from hormonal treatment or cell line heterogeneity. Relevant clusters of genes that can discriminate between [PIP+] and [PIP-] cells were identified. Functional and regulatory network analyses based on a knowledge database revealed a master network of PIP co-modulated genes, including many interconnecting oncogenes and tumor suppressor genes, half of which were detected as differentially expressed through high-precision measurements. The network identified appears associated with an inhibition of proliferation coupled with an increase of apoptosis and an enhancement of cell adhesion in breast cancer cell lines, and contains many genes with a STAT5 regulatory motif in their promoters.<h4>Conclusions</h4>Our global exploratory approach identified biological pathways modulated along with PIP expression, providing further support for its good prognostic value of disease-free survival in breast cancer. Moreover, our data pointed to the importance of a regulatory subnetwork associated with PIP expression in which STAT5 appears as a potential transcriptional regulator.Marie-Anne DebilySandrine El MarhomyVirginie BoulangerEric EvenoRégine Mariage-SamsonAlessandra CamarcaCharles AuffrayDominique Piatier-TonneauSandrine ImbeaudPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 3, p e4696 (2009)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Marie-Anne Debily
Sandrine El Marhomy
Virginie Boulanger
Eric Eveno
Régine Mariage-Samson
Alessandra Camarca
Charles Auffray
Dominique Piatier-Tonneau
Sandrine Imbeaud
A functional and regulatory network associated with PIP expression in human breast cancer.
description <h4>Background</h4>The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted combined gene expression profiling and network analysis studies on selected breast cancer cell lines presenting distinct PIP expression levels and hormonal receptor status, to explore the functional and regulatory network of PIP co-modulated genes.<h4>Principal findings</h4>Microarray analysis allowed identification of genes co-modulated with PIP independently of modulations resulting from hormonal treatment or cell line heterogeneity. Relevant clusters of genes that can discriminate between [PIP+] and [PIP-] cells were identified. Functional and regulatory network analyses based on a knowledge database revealed a master network of PIP co-modulated genes, including many interconnecting oncogenes and tumor suppressor genes, half of which were detected as differentially expressed through high-precision measurements. The network identified appears associated with an inhibition of proliferation coupled with an increase of apoptosis and an enhancement of cell adhesion in breast cancer cell lines, and contains many genes with a STAT5 regulatory motif in their promoters.<h4>Conclusions</h4>Our global exploratory approach identified biological pathways modulated along with PIP expression, providing further support for its good prognostic value of disease-free survival in breast cancer. Moreover, our data pointed to the importance of a regulatory subnetwork associated with PIP expression in which STAT5 appears as a potential transcriptional regulator.
format article
author Marie-Anne Debily
Sandrine El Marhomy
Virginie Boulanger
Eric Eveno
Régine Mariage-Samson
Alessandra Camarca
Charles Auffray
Dominique Piatier-Tonneau
Sandrine Imbeaud
author_facet Marie-Anne Debily
Sandrine El Marhomy
Virginie Boulanger
Eric Eveno
Régine Mariage-Samson
Alessandra Camarca
Charles Auffray
Dominique Piatier-Tonneau
Sandrine Imbeaud
author_sort Marie-Anne Debily
title A functional and regulatory network associated with PIP expression in human breast cancer.
title_short A functional and regulatory network associated with PIP expression in human breast cancer.
title_full A functional and regulatory network associated with PIP expression in human breast cancer.
title_fullStr A functional and regulatory network associated with PIP expression in human breast cancer.
title_full_unstemmed A functional and regulatory network associated with PIP expression in human breast cancer.
title_sort functional and regulatory network associated with pip expression in human breast cancer.
publisher Public Library of Science (PLoS)
publishDate 2009
url https://doaj.org/article/49cd927f14db420e84bfb7dc6d834b96
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