Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-10-16
pubmed:abstractText
The goal of the present study is to unveil the gene expression profile specific to the biological processes of human breast epithelial cell invasion and migration using an MCF10A model genetically engineered to constitutively activate the H-ras or N-ras signaling pathway. We previously showed that H-Ras, but not N-Ras, induces MCF10A cell invasion/migration, whereas both H-Ras and N-Ras induce cell proliferation and phenotypic transformation. Thus, these cell lines provide an experimental system to separate the gene expression profile associated with cell invasion apart from cell proliferation/transformation. Analysis of whole human genome microarray revealed that 412 genes were differentially expressed among MCF10A, N-Ras MCF10A, and H-Ras MCF10A cells and hierarchical clustering separated 412 genes into four clusters. We then tested whether S100A8 and S100A9, two of the genes which are most highly up-regulated in an H-Ras-specific manner, play a causative role for H-Ras-mediated MCF10A cell invasion and migration. Importantly, small interfering RNA-mediated knockdown of S100A8/A9 expression significantly reduced H-Ras-induced invasion/migration. Conversely, the induction of S100A8/A9 expression conferred the invasive/migratory phenotype to parental MCF10A cells. Furthermore, we provided evidence of signaling cross-talk between S100A8/A9 and the mitogen-activated protein kinase signaling pathways essential for H-Ras-mediated cell invasion and migration. Taken together, this study revealed S100A8/A9 genes as candidate markers for metastatic potential of breast epithelial cells. Our gene profile data provide useful information which may lead to the identification of additional potential targets for the prognosis and/or therapy of metastatic breast cancer.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1541-7786
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1544-53
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18922970-Breast, pubmed-meshheading:18922970-Calcium, pubmed-meshheading:18922970-Calgranulin A, pubmed-meshheading:18922970-Calgranulin B, pubmed-meshheading:18922970-Cell Movement, pubmed-meshheading:18922970-Cell Transformation, Neoplastic, pubmed-meshheading:18922970-Cluster Analysis, pubmed-meshheading:18922970-Epithelial Cells, pubmed-meshheading:18922970-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:18922970-Gene Expression Profiling, pubmed-meshheading:18922970-Gene Expression Regulation, pubmed-meshheading:18922970-Humans, pubmed-meshheading:18922970-Matrix Metalloproteinase 2, pubmed-meshheading:18922970-Matrix Metalloproteinase 9, pubmed-meshheading:18922970-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:18922970-Phenotype, pubmed-meshheading:18922970-Proto-Oncogene Proteins p21(ras), pubmed-meshheading:18922970-Reproducibility of Results, pubmed-meshheading:18922970-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18922970-Tumor Markers, Biological, pubmed-meshheading:18922970-p38 Mitogen-Activated Protein Kinases
pubmed:year
2008
pubmed:articleTitle
Global gene expression profiling unveils S100A8/A9 as candidate markers in H-ras-mediated human breast epithelial cell invasion.
pubmed:affiliation
College of Pharmacy, Duksung Women's University, Seoul, Korea. armoon@duksung.ac.kr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural