NDLI: Genomic amplification and oncogenic properties of the GASC1 histone demethylase gene in breast cancer

Content Provider	PubMed Central
Author	Liu, Gang Bollig-fischer, Aliccia Bas, Kreike Vijver, Marc J. Van De Abrams, Judith Ethier, Stephen P. Yang, Zeng-quan
Abstract	Previously, mapping of the 9p23-24 amplicon in esophageal cancer cell lines led us to the positional cloning of GASC1 (gene amplified in squamous cell carcinoma 1), which encodes a nuclear protein with a Jumonji C (JmjC) domain that catalyzes lysine (K) demethylation of histones. However, the transforming roles of GASC1 in breast cancer remain to be determined. In this study, we identified GASC1 as one of the amplified genes for the 9p23-24 region in breast cancer, particularly in basal-like subtypes. The levels of GASC1 transcript expression were significantly higher in aggressive, basal-like breast cancers compared with non basal-like breast cancers. Our in vitro assays demonstrated that GASC1 induces transformed phenotypes, including growth factor-independent proliferation, anchorage-independent growth, altered morphogenesis in Matrigel, and mammosphere forming ability, when over expressed in immortalized, nontransformed mammary epithelial MCF10A cells. Additionally, GASC1 demethylase activity regulates the expression of genes critical for stem cell self-renewal, including NOTCH1, and may be linked to the stem cell phenotypes in breast cancer. Thus, GASC1 is a driving oncogene in the 9p23-24 amplicon in human breast cancer and targeted inhibition of GASC1 histone demethylase in cancer could provide potential new avenues for therapeutic development.
Related Links	http://dx.doi.org/10.1038/onc.2009.297
Ending Page	4500
Page Count	10
Starting Page	4491
File Format	PDF
ISSN	09509232
e-ISSN	14765594
Journal	Oncogene
Issue Number	50
Volume Number	28
Language	English
Publisher Date	2009-12-17
Access Restriction	Open
Subject Keyword	Genetics Cancer Research Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics Molecular Biology Cancer Research

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