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Alterations in the gene expression profile of MCF‐7 breast tumor cells in response to c‐Jun
Author(s) -
RinehartKim Janet,
Johnston Melissa,
Birrer Michael,
Bos Timothy
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001015)88:2<180::aid-ijc6>3.0.co;2-h
Subject(s) - gene , c jun , biology , phenotype , gene expression , microbiology and biotechnology , downregulation and upregulation , regulation of gene expression , genetics , cancer research , transcription factor
MCF7 breast tumor cells overexpressing human c‐Jun exhibit a transformed phenotype characterized not only by increased tumorigenicity but also by enhanced motility and invasion. The cellular phenotypic response to c‐Jun overexpression is likely due, at least in part, to altered patterns of gene expression. In order to begin to understand the complexities by which elevated production of c‐Jun alters the state of the cell, we have profiled the expression of 588 different genes by comparative hybridization. By using this approach, we have identified a total of 21 upregulated or downregulated gene targets responsive to c‐Jun overexpression. Interestingly, 8 of these genes have been previously found associated with c‐Jun or AP‐1 activity and therefore provide internal validation for this approach to target gene discovery. The remaining 13 genes represent potential new c‐Jun regulated target genes. Genomic sequence information was available for 15 of the 21 genes identified in this screen. Analysis of these genomic sequences revealed the presence of AP‐1 or AP‐1‐like sequences in 12 of the 15 genes examined. Consistent with a direct mechanism of target regulation by c‐Jun, gel shift analysis of selected AP‐1‐containing promoter regions revealed elevated and specific binding by proteins present in nuclear extracts of c‐Jun expressing MCF7 cells. Int. J. Cancer 88:180–190, 2000. © 2000 Wiley‐Liss, Inc.