RNAi profiling of human ezh2 specific siRNA A673 treated cells reveals EZh2 is a mediator of EWS-FLI1 driven tumor growth blocking endothelial and neuro-ectodermal differentiation

ABSTRACT: Ewing Tumors (ET) are highly malignant tumors, localized in bone or soft tissue and are molecularly defined by ews/ets translocations. We identified histone methyl-transferase Enhancer of Zeste, Drosophila, Homolog 2 (EZH2) to be increased in ET. EZH2’s suppressive activity maintains stemness in normal and malignant cells. Here we found EZH2 to be upregulated by the pathognomonic fusion oncogene EWS-FLI1 in ET and mesenchymal stem cells. Downregulation of EZH2 by RNA interference in ET suppressed oncogenic transformation by inhibiting clonogenicity in vitro. Similarly, tumor development and metastasis in immunodeficient Rag2-/-γC-/- mice was suppressed. EZH2-mediated gene silencing was shown to be dependent on histone deacetylase (HDAC) activity. Subsequent microarray analysis of EZH2 k

ORGANISM(S): Homo sapiens

SUBMITTER: Guenther Richter 

PROVIDER: E-GEOD-12692 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress