ODAM Expression Inhibits Human Breast Cancer Tumorigenesis

We have posited that Odontogenic Ameloblast Associated Protein (ODAM) serves as a novel prognostic biomarker in breast cancer and now have investigated its potential role in regulating tumor growth and metastasis. Human breast cancer MDA-MB-231 cells were transfected with a recombinant ODAM plasmid...

Full description

Bibliographic Details
Main Authors: Daniel P. Kestler, James S. Foster, Charles T. Bruker, John W. Prenshaw, Stephen J. Kennel, Jonathan S. Wall, Deborah T. Weiss, Alan Solomon
Format: Article
Language:English
Published: SAGE Publishing 2011-01-01
Series:Breast Cancer: Basic and Clinical Research
Online Access:https://doi.org/10.4137/BCBCR.S6859
_version_ 1819264854394929152
author Daniel P. Kestler
James S. Foster
Charles T. Bruker
John W. Prenshaw
Stephen J. Kennel
Jonathan S. Wall
Deborah T. Weiss
Alan Solomon
author_facet Daniel P. Kestler
James S. Foster
Charles T. Bruker
John W. Prenshaw
Stephen J. Kennel
Jonathan S. Wall
Deborah T. Weiss
Alan Solomon
author_sort Daniel P. Kestler
collection DOAJ
description We have posited that Odontogenic Ameloblast Associated Protein (ODAM) serves as a novel prognostic biomarker in breast cancer and now have investigated its potential role in regulating tumor growth and metastasis. Human breast cancer MDA-MB-231 cells were transfected with a recombinant ODAM plasmid construct (or, as a control, the plasmid vector alone). ODAM expression increased adhesion and apoptosis of the transfected MDA-MB-231 cells and suppressed their growth rate, migratory activity, and capability to invade extracellular matrix-coated membranes. Implantation of such cells into mouse mammary fat pads resulted in significantly smaller tumors than occurred in animals that received control cells; furthermore, ODAM-expressing cells, when injected intravenously into mice, failed to metastasize, whereas the control-transfected counterparts produced extensive lung lesions. Our finding that induction of ODAM expression in human breast cancer cells markedly inhibited their neoplastic properties provides further evidence for the regulatory role of this molecule in tumorigenesis and, consequently, is of potential clinical import.
first_indexed 2024-12-23T20:36:06Z
format Article
id doaj.art-7a028c5b4c154dd9a4f6c907581e1feb
institution Directory Open Access Journal
issn 1178-2234
language English
last_indexed 2024-12-23T20:36:06Z
publishDate 2011-01-01
publisher SAGE Publishing
record_format Article
series Breast Cancer: Basic and Clinical Research
spelling doaj.art-7a028c5b4c154dd9a4f6c907581e1feb2022-12-21T17:32:05ZengSAGE PublishingBreast Cancer: Basic and Clinical Research1178-22342011-01-01510.4137/BCBCR.S6859ODAM Expression Inhibits Human Breast Cancer TumorigenesisDaniel P. Kestler0James S. Foster1Charles T. Bruker2John W. Prenshaw3Stephen J. Kennel4Jonathan S. Wall5Deborah T. Weiss6Alan Solomon7Human Immunology and Cancer Program/Department of MedicineHuman Immunology and Cancer Program/Department of MedicineDepartment of Pathology, University of Tennessee Graduate School of Medicine, Knoxville, Tennessee, USA.University of Tennessee College of Medicine, Memphis, Tennessee, USA.Human Immunology and Cancer Program/Department of MedicineHuman Immunology and Cancer Program/Department of MedicineHuman Immunology and Cancer Program/Department of MedicineHuman Immunology and Cancer Program/Department of MedicineWe have posited that Odontogenic Ameloblast Associated Protein (ODAM) serves as a novel prognostic biomarker in breast cancer and now have investigated its potential role in regulating tumor growth and metastasis. Human breast cancer MDA-MB-231 cells were transfected with a recombinant ODAM plasmid construct (or, as a control, the plasmid vector alone). ODAM expression increased adhesion and apoptosis of the transfected MDA-MB-231 cells and suppressed their growth rate, migratory activity, and capability to invade extracellular matrix-coated membranes. Implantation of such cells into mouse mammary fat pads resulted in significantly smaller tumors than occurred in animals that received control cells; furthermore, ODAM-expressing cells, when injected intravenously into mice, failed to metastasize, whereas the control-transfected counterparts produced extensive lung lesions. Our finding that induction of ODAM expression in human breast cancer cells markedly inhibited their neoplastic properties provides further evidence for the regulatory role of this molecule in tumorigenesis and, consequently, is of potential clinical import.https://doi.org/10.4137/BCBCR.S6859
spellingShingle Daniel P. Kestler
James S. Foster
Charles T. Bruker
John W. Prenshaw
Stephen J. Kennel
Jonathan S. Wall
Deborah T. Weiss
Alan Solomon
ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
Breast Cancer: Basic and Clinical Research
title ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
title_full ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
title_fullStr ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
title_full_unstemmed ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
title_short ODAM Expression Inhibits Human Breast Cancer Tumorigenesis
title_sort odam expression inhibits human breast cancer tumorigenesis
url https://doi.org/10.4137/BCBCR.S6859
work_keys_str_mv AT danielpkestler odamexpressioninhibitshumanbreastcancertumorigenesis
AT jamessfoster odamexpressioninhibitshumanbreastcancertumorigenesis
AT charlestbruker odamexpressioninhibitshumanbreastcancertumorigenesis
AT johnwprenshaw odamexpressioninhibitshumanbreastcancertumorigenesis
AT stephenjkennel odamexpressioninhibitshumanbreastcancertumorigenesis
AT jonathanswall odamexpressioninhibitshumanbreastcancertumorigenesis
AT deborahtweiss odamexpressioninhibitshumanbreastcancertumorigenesis
AT alansolomon odamexpressioninhibitshumanbreastcancertumorigenesis