Background: PcG protein BMI1 is transcriptionally regulated by Myc and is up-regulated in cancer cells. Results:The WNT pathway plays an important role in Myc regulation of BMI1. Conclusion: BMI1 up-regulates the WNT pathway, which in turn regulates expression of BMI1 via c-Myc. Significance: The study provides insights into the regulation of BMI1 and suggests that BMI1 expression may be targeted by WNT inhibitors in cancer cells.

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We show that receptor induced G protein βγ subunit translocation from the plasma membrane to the Golgi allows a receptor to initiate fragmentation and regulate secretion. A lung epithelial cell line, A549, was shown to contain an endogenous translocating G protein γ subunit and exhibit receptor-induced Golgi fragmentation. Receptor-induced Golgi fragmentation was inhibited by a shRNA specific to the endogenous translocating γ subunit. A kinase defective protein kinase D and a phospholipase C β inhibitor blocked receptor-induced Golgi fragmentation, suggesting a role for this process in secretion. Consistent with βγ translocation dependence, fragmentation induced by receptor activation was inhibited by a dominant negative nontranslocating γ3. Insulin secretion was shown to be induced by muscarinic receptor activation in a pancreatic β cell line, NIT-1. Induction of insulin secretion was also inhibited by the dominant negative γ3 subunit consistent with the Golgi fragmentation induced by βγ complex translocation playing a role in secretion.G protein-coupled receptors | live cell imaging | signaling | insulin