E-GEOD-46251 - Microarray data of human leukemia cells MV4;11 with or without IKK inhibitor treatment.
Released on 19 September 2013, last updated on 30 September 2013
MLL fusion proteins in leukemia induce aberrant transcriptional elongation and associated chromatin perturbations, however the upstream signaling pathways and activators that recruit or retain MLL oncoproteins at initiated promoters are unknown. Through functional and comparative genomic studies, we identified an essential role for NF-kB signaling in MLL leukemia. Suppression of NF-kB led to robust anti-leukemia effects that phenocopied loss of functional MLL oncoprotein or associated epigenetic cofactors. The NF-kB subunit RELA occupies promoter regions of crucial MLL target genes and sustains the MLL-dependent leukemia stem cell program. IKK/NF-kB signaling is required for wild-type MLL and fusion protein retention and maintenance of associated histone modifications providing a molecular rationale for enhanced efficacy in therapeutic targeting of this pathway in MLL leukemias. MV4;11 cells were treated with 1µM IKK inhibitor or vehicle. Each group contains triplicate samples
transcription profiling by array
HSU-PING KUO <firstname.lastname@example.org>, Dung-Fang Lee, Hsu-Ping Kuo, Ihor R Lemischka, Jesus Duque-Afonso, Jie Su, Maria E Figueroa, Masayuki Iwasaki, Michael L Cleary, Stephen H Wong, Zhong Wang