An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells

<p>Abstract</p> <p>Background</p> <p>The sex hormone estrogen (E2) is pivotal to normal mammary gland growth and differentiation and in breast carcinogenesis. In this <it>in silico </it>study, we examined metabolic differences between ER(+)ve breast cancer c...

Full description

Bibliographic Details
Main Authors: Davie James R, Mandal Soma
Format: Article
Language:English
Published: BMC 2007-09-01
Series:BMC Cancer
Online Access:http://www.biomedcentral.com/1471-2407/7/181
_version_ 1819138403219800064
author Davie James R
Mandal Soma
author_facet Davie James R
Mandal Soma
author_sort Davie James R
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p>The sex hormone estrogen (E2) is pivotal to normal mammary gland growth and differentiation and in breast carcinogenesis. In this <it>in silico </it>study, we examined metabolic differences between ER(+)ve breast cancer cells during E2 deprivation.</p> <p>Methods</p> <p>Public repositories of SAGE and MA gene expression data generated from E2 deprived ER(+)ve breast cancer cell lines, MCF-7 and ZR75-1 were compared with normal breast tissue. We analyzed gene ontology (GO), enrichment, clustering, chromosome localization, and pathway profiles and performed multiple comparisons with cell lines and tumors with different ER status.</p> <p>Results</p> <p>In all GO terms, biological process (BP), molecular function (MF), and cellular component (CC), MCF-7 had higher gene utilization than ZR75-1. Various analyses showed a down-regulated immune function, an up-regulated protein (ZR75-1) and glucose metabolism (MCF-7). A greater percentage of 77 common genes localized to the q arm of all chromosomes, but in ZR75-1 chromosomes 11, 16, and 19 harbored more overexpressed genes. Despite differences in gene utilization (electron transport, proteasome, glycolysis/gluconeogenesis) and expression (ribosome) in both cells, there was an overall similarity of ZR75-1 with ER(-)ve cell lines and ER(+)ve/ER(-)ve breast tumors.</p> <p>Conclusion</p> <p>This study demonstrates integral metabolic differences may exist within the same cell subtype (luminal A) in representative ER(+)ve cell line models. Selectivity of gene and pathway usage for strategies such as energy requirement minimization, sugar utilization by ZR75-1 contrasted with MCF-7 cells, expressing genes whose protein products require ATP utilization. Such characteristics may impart aggressiveness to ZR75-1 and may be prognostic determinants of ER(+)ve breast tumors.</p>
first_indexed 2024-12-22T11:06:13Z
format Article
id doaj.art-6f242e7348f84d628a9e8b107967f4a7
institution Directory Open Access Journal
issn 1471-2407
language English
last_indexed 2024-12-22T11:06:13Z
publishDate 2007-09-01
publisher BMC
record_format Article
series BMC Cancer
spelling doaj.art-6f242e7348f84d628a9e8b107967f4a72022-12-21T18:28:19ZengBMCBMC Cancer1471-24072007-09-017118110.1186/1471-2407-7-181An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cellsDavie James RMandal Soma<p>Abstract</p> <p>Background</p> <p>The sex hormone estrogen (E2) is pivotal to normal mammary gland growth and differentiation and in breast carcinogenesis. In this <it>in silico </it>study, we examined metabolic differences between ER(+)ve breast cancer cells during E2 deprivation.</p> <p>Methods</p> <p>Public repositories of SAGE and MA gene expression data generated from E2 deprived ER(+)ve breast cancer cell lines, MCF-7 and ZR75-1 were compared with normal breast tissue. We analyzed gene ontology (GO), enrichment, clustering, chromosome localization, and pathway profiles and performed multiple comparisons with cell lines and tumors with different ER status.</p> <p>Results</p> <p>In all GO terms, biological process (BP), molecular function (MF), and cellular component (CC), MCF-7 had higher gene utilization than ZR75-1. Various analyses showed a down-regulated immune function, an up-regulated protein (ZR75-1) and glucose metabolism (MCF-7). A greater percentage of 77 common genes localized to the q arm of all chromosomes, but in ZR75-1 chromosomes 11, 16, and 19 harbored more overexpressed genes. Despite differences in gene utilization (electron transport, proteasome, glycolysis/gluconeogenesis) and expression (ribosome) in both cells, there was an overall similarity of ZR75-1 with ER(-)ve cell lines and ER(+)ve/ER(-)ve breast tumors.</p> <p>Conclusion</p> <p>This study demonstrates integral metabolic differences may exist within the same cell subtype (luminal A) in representative ER(+)ve cell line models. Selectivity of gene and pathway usage for strategies such as energy requirement minimization, sugar utilization by ZR75-1 contrasted with MCF-7 cells, expressing genes whose protein products require ATP utilization. Such characteristics may impart aggressiveness to ZR75-1 and may be prognostic determinants of ER(+)ve breast tumors.</p>http://www.biomedcentral.com/1471-2407/7/181
spellingShingle Davie James R
Mandal Soma
An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
BMC Cancer
title An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
title_full An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
title_fullStr An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
title_full_unstemmed An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
title_short An integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
title_sort integrated analysis of genes and pathways exhibiting metabolic differences between estrogen receptor positive breast cancer cells
url http://www.biomedcentral.com/1471-2407/7/181
work_keys_str_mv AT daviejamesr anintegratedanalysisofgenesandpathwaysexhibitingmetabolicdifferencesbetweenestrogenreceptorpositivebreastcancercells
AT mandalsoma anintegratedanalysisofgenesandpathwaysexhibitingmetabolicdifferencesbetweenestrogenreceptorpositivebreastcancercells
AT daviejamesr integratedanalysisofgenesandpathwaysexhibitingmetabolicdifferencesbetweenestrogenreceptorpositivebreastcancercells
AT mandalsoma integratedanalysisofgenesandpathwaysexhibitingmetabolicdifferencesbetweenestrogenreceptorpositivebreastcancercells