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Profile of differentially expressed genes after transfer of chromosome 17 into the breast cancer cell line CAl51
Author(s) -
Klebig Christiane,
Seitz Susanne,
Korsching Eberhard,
Kristiansen Glen,
Gustavus Dirk,
Scherneck Siegfried,
Petersen Iver
Publication year - 2005
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.20240
Subject(s) - biology , carcinogenesis , suppression subtractive hybridization , gene , breast cancer , cancer research , microarray analysis techniques , microbiology and biotechnology , phenotype , gene expression , genetics , cancer , cdna library
Previous studies have shown that transfer of chromosome 17 suppresses the tumorigenic phenotype of the breast cancer cell line CAL51, suggesting the presence of putative tumor suppressor genes on this chromosome. Suppression subtractive hybridization and oligonucleotide microarray analyses were performed to identify differentially expressed genes in nontumorigenic microcell hybrids, CAL/17‐1 and CAL/17‐3, when compared with CAL51 cells. In total, 263 differentially expressed transcripts were associated with these phenotypes. Of these, a high percentage is involved in various biological processes associated with tumorigenesis, including DNA‐dependent regulation of transcription, regulation of cell cycle, signal transduction, and cell proliferation. Microarray analysis of selected chromosome 17 genes in a series of 25 human primary breast tumors showed associations with clinicopathologic parameters of the tumors. Of these genes, TOB1 (transducer of ERBB2 ) was selected for further expression analysis. Using RT‐PCR and immunohistochemical staining of tissue microarrays, we could reveal a differential mRNA and protein expression of TOB1 in the majority of breast tumors and lymph node metastases compared with normal breast tissues, indicating a potential role of this protein in breast tumorigenesis. © 2005 Wiley‐Liss, Inc.