Expression data from Bmi1-overexpressing Ink4a-Arf-null hepatoblasts

Forced expression of Bmi1 accelerated the self-renewal of hepatic stem/progenitor cells and eventually induced their transformation in an in vivo transplant model. The Ink4a/Arf locus, which encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf, is a pivotal target of Bmi1. Therefore, it would be of importance to understand the contribution of the Ink4a/Arf locus to Bmi1 oncogenic functions in cancer and search for as-yet-unknown Bmi1 target genes other than Ink4a/Arf. We used microarrays to explore novel candidate downstream targets for Bmi1 in hepatic stem/progenitor cells Purified Dlk-positive hepatoblasts at day 28 of culture were subjected to RNA extraction and hybridization on Affymetrix microarrays. Data were obtained for quadrant samples from four independent experiments.