FL5.12 Bfl-1DC/p53DD-derived splenic tumors compared to the parental FL5.12 Bfl-1DC/p53DD cell line

ABSTRACT: The antiapoptotic Bcl-2 family member Bfl-1 is upregulated in many human tumors in which NF-kB is implicated, and contributes significantly to tumor cell survival and chemoresistance. We previously found that NF-kB induces transcription of bfl-1, and that the Bfl-1 protein is also regulated by the ubiquitin-proteasome. However little is known of the role that dysregulation of Bfl-1 turnover plays in cancer. We found that ubiquitination-resistant mutants of Bfl-1 display increased stability and greatly accelerate tumor formation in a mouse model of leukemia/lymphoma. Gene expression profiling revealed that tyrosine kinase Lck is highly upregulated and activated in these tumors compared to the parental cells, as were several genes in the RANK signaling pathway, and leads to activation of the

ORGANISM(S): Mus musculus

SUBMITTER: Jérôme Kucharczak 

PROVIDER: E-GEOD-18204 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress