Bmi1 induces telomerase activity and immortalizes human mammary epithelial cells. Bmi1 extends the replicative life span of human fibroblasts by suppressing the p16-dependent senescence pathway. It has also been termed an oncogene with aberrant expression in various carcinomas. It has been shown to be a negative regulator of p19Arf, Ink4a (p14Arf) and tp53 known tumor repressors. Ablation of Bmi1 is required for short term survival of cancer cells.
In addition, Bmi1 expression promotes HSC self-renewal. These findings highlight the importance of epigenetic regulation in HSC self-renewal and identify PcG genes as potential targets for therapeutic HSC manipulation.
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