Gene expression data from MGHU3 bladder cancer cells (FGFR3-Y375C) treated with TAK1 siRNA and/or PD173074

ABSTRACT: The NFM-NM-:B transcription factor is constitutively active in a number of hematologic and solid tumors, and many signaling pathways implicated in cancer are likely connected to NFM-NM-:B activation. A critical mediator of NFM-NM-:B activity is TGFM-NM-2-activated kinase 1 (TAK1). Here, we identify TAK1 as a novel interacting protein and direct target of fibroblast growth factor receptor 3 (FGFR3) tyrosine kinase activity. We further demonstrate that activating mutations in FGFR3 associated with both multiple myeloma and bladder cancer can modulate expression of genes which regulate NFM-NM-:B signaling, and promote both NFM-NM-:B transcriptional activity and cell adhesion in a manner dependent on TAK1 expression in both cancer cell types. Our findings suggest TAK1 as a potential therape

ORGANISM(S): Homo sapiens

SUBMITTER: Leslie Thompson 

PROVIDER: E-GEOD-52452 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress