WISP-2 as a novel estrogen-responsive gene in human breast cancer cells.
In order to search for novel estrogen-responsive genes, we performed serial analysis of gene expression (SAGE) for estrogen-treated MCF-7 human breast cancer cells. SAGE analysis of 31,000 and 30,856 tags from non-treated and 17 beta-estradiol (E2)-treated cells for 24 h, respectively, facilitated the identification of 15,037 different transcripts. Comparison of these two SAGE libraries indicated a remarkable similarity in expression profiles. Among the identified transcripts, four genes were found to be markedly increased for E2-treated cells compared with control cells. Three of the transcripts were cathepsin D, pS2 and high mobility group 1 protein, which have been described as estrogen-inducible genes. The fourth gene was WISP-2 (Wnt-1 inducible signaling pathway protein 2) which has recently been reported as an up-regulated gene in the mammary epithelial cell line C57 MG transformed by the Wnt-1 oncogene. The increase in WISP-2 mRNA was completely prevented by co-incubation with a pure anti-estrogen ICI 182,780, but not by coincubation with cycloheximide, indicating that WISP-2 is directly regulated by the estrogen receptor. The WISP-2 gene was also induced by treating with environmental estrogens, such as bisphenol-A or nonylphenol. This study represents the first comprehensive gene expression analysis of estrogen-treated human breast cancer cells.
Inadera
H
H
Department of Molecular Preventive Medicine, School of Medicine and Environmental Science Center, CREST, University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Hashimoto
S
S
Dong
H Y
HY
Suzuki
T
T
Nagai
S
S
Yamashita
T
T
Toyoda
N
N
Matsushima
K
K
D000395:Air Pollutants, Occupational / Q000494:pharmacology; D001559:Benzhydryl Compounds; D001943:Breast Neoplasms / Q000235:genetics*; D055511:CCN Intercellular Signaling Proteins; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology*; D020847:Estrogen Receptor Modulators / Q000494:pharmacology; D005260:Female; D000077267:Fulvestrant; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D007633:Keratins / Q000235:genetics; D009363:Neoplasm Proteins / Q000235:genetics; D010636:Phenols / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics*; D014407:Tumor Cells, Cultured; D000098826:Bisphenol A Compounds
D000395:Air Pollutants, Occupational; D001559:Benzhydryl Compounds; D055511:CCN Intercellular Signaling Proteins; D003513:Cycloheximide; D003609:Dactinomycin; D004958:Estradiol; D020847:Estrogen Receptor Modulators; D000077267:Fulvestrant; D036341:Intercellular Signaling Peptides and Proteins; D007633:Keratins; D009363:Neoplasm Proteins; D010636:Phenols; D012333:RNA, Messenger; D012097:Repressor Proteins; D014157:Transcription Factors; C413323:CCN5 protein, human; C025256:nonylphenol; C006780:bisphenol A; D000098826:Bisphenol A Compounds