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E-GEOD-74970 - Histone deacetylase inhibitors antagonize distinct pathways to suppress tumorigenesis of embryonal rhabdomyosarcoma

Released on 21 December 2015, last updated on 26 December 2015
Homo sapiens
Samples (12)
Array (1)
Protocols (5)
Embryonal rhabdomyosarcoma (ERMS) is the most common soft tissue cancer in children and is characterized by myogenic differentiation arrest. The prognosis of patients with relapsed or metastatic disease remains poor. ERMS genomes show few recurrent mutations, suggesting that other molecular mechanisms such as epigenetic regulation might play major role in driving ERMS tumor biology. In this study, we have demonstrated the diverse roles of HDACs in the pathogenesis of ERMS by characterizing effects of HDAC inhibitors, trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA; also known as vorinostat) in vitro and in vivo. TSA and SAHA suppress ERMS tumor growth and progression by inducing myogenic differentiation as well as reducing the self-renewal and migratory capacity of ERMS cells. To identify candidate genes that are differentially regulated in histone deacetylase inhibitor-treated embryonal rhabdomyosarcoma, a gene expression profiling study using the Affymetrix Human Gene 2.0 microarray platform and ingenuity pathway analysis of differentially expressed genes were performed on RD and 381T cells treated with trichostatin A or dimethyl sulfoxide (treatment vehicle).
Experiment type
transcription profiling by array 
James William MacDonald <>, Eleanor Y Chen, Isaac Jenkins, James W MacDonald, Michael Phelps, Terra Vleeshouwer-Neumann, Theo K Bammler
Investigation descriptionE-GEOD-74970.idf.txt
Sample and data relationshipE-GEOD-74970.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-GEOD-16686.adf.txt