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Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells

BACKGROUND: Osteopontin is a secreted, integrin-binding and phosphorylated acidic glycoprotein which has an important role in tumor progression. FINDINGS: In this study, we have utilized suppressive subtractive hybridization (SSH) to evaluate OPN regulated gene expression, using the Rama 37 benign n...

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Autores principales: Kurisetty, Vittal V, Johnston, Patrick G, Rudland, Philip S, El-Tanani, Mohamed K
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644310/
https://www.ncbi.nlm.nih.gov/pubmed/19192273
http://dx.doi.org/10.1186/1756-0500-2-15
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author Kurisetty, Vittal V
Johnston, Patrick G
Rudland, Philip S
El-Tanani, Mohamed K
author_facet Kurisetty, Vittal V
Johnston, Patrick G
Rudland, Philip S
El-Tanani, Mohamed K
author_sort Kurisetty, Vittal V
collection PubMed
description BACKGROUND: Osteopontin is a secreted, integrin-binding and phosphorylated acidic glycoprotein which has an important role in tumor progression. FINDINGS: In this study, we have utilized suppressive subtractive hybridization (SSH) to evaluate OPN regulated gene expression, using the Rama 37 benign non-invasive rat mammary cell line and a subclone, Rama 37-OPN. Rama 37-OPN was produced by stably transfecting Rama 37 with an OPN expression vector and it demonstrates increased malignant properties in vitro. Sequence and expression array analysis of the respective cDNA libraries of over 1600 subtracted cDNA fragments revealed 982 ESTs, 45 novel sequences and 659 known genes. The known up-regulated genes in the Rama 37-OPN library code for proteins with a variety of functions including those involved in metabolism, cell adhesion and migration, signal transduction and in apoptosis. Four of the most differentially expressed genes between the benign and in vitro malignant rat mammary cell lines are tumor protein translationally controlled I (TPTI), aryl hydrocarbon receptor nuclear translocator (ARNT), ataxia telangiectasia mutated (ATM) and RAN GTPase (RAN). The largest difference (ca 10,000 fold) between the less aggressively (MCF-7, ZR-75) and more aggressively malignant (MDA MB 231, MDA MB 435S) human breast cancer cell lines is that due to RAN, the next is that due to osteopontin itself. CONCLUSION: The results suggest that enhanced properties associated with the malignant state in vitro induced by osteopontin may be due to, in part, overexpression of RAN GTPase and these biological results are the subject of a subsequent publication [1].
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spelling pubmed-26443102009-02-18 Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells Kurisetty, Vittal V Johnston, Patrick G Rudland, Philip S El-Tanani, Mohamed K BMC Res Notes Data Note BACKGROUND: Osteopontin is a secreted, integrin-binding and phosphorylated acidic glycoprotein which has an important role in tumor progression. FINDINGS: In this study, we have utilized suppressive subtractive hybridization (SSH) to evaluate OPN regulated gene expression, using the Rama 37 benign non-invasive rat mammary cell line and a subclone, Rama 37-OPN. Rama 37-OPN was produced by stably transfecting Rama 37 with an OPN expression vector and it demonstrates increased malignant properties in vitro. Sequence and expression array analysis of the respective cDNA libraries of over 1600 subtracted cDNA fragments revealed 982 ESTs, 45 novel sequences and 659 known genes. The known up-regulated genes in the Rama 37-OPN library code for proteins with a variety of functions including those involved in metabolism, cell adhesion and migration, signal transduction and in apoptosis. Four of the most differentially expressed genes between the benign and in vitro malignant rat mammary cell lines are tumor protein translationally controlled I (TPTI), aryl hydrocarbon receptor nuclear translocator (ARNT), ataxia telangiectasia mutated (ATM) and RAN GTPase (RAN). The largest difference (ca 10,000 fold) between the less aggressively (MCF-7, ZR-75) and more aggressively malignant (MDA MB 231, MDA MB 435S) human breast cancer cell lines is that due to RAN, the next is that due to osteopontin itself. CONCLUSION: The results suggest that enhanced properties associated with the malignant state in vitro induced by osteopontin may be due to, in part, overexpression of RAN GTPase and these biological results are the subject of a subsequent publication [1]. BioMed Central 2009-02-03 /pmc/articles/PMC2644310/ /pubmed/19192273 http://dx.doi.org/10.1186/1756-0500-2-15 Text en Copyright © 2009 El-Tanani et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Data Note
Kurisetty, Vittal V
Johnston, Patrick G
Rudland, Philip S
El-Tanani, Mohamed K
Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title_full Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title_fullStr Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title_full_unstemmed Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title_short Identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
title_sort identification of genes differentially expressed between benign and osteopontin transformed rat mammary epithelial cells
topic Data Note
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644310/
https://www.ncbi.nlm.nih.gov/pubmed/19192273
http://dx.doi.org/10.1186/1756-0500-2-15
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