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Functional Interactions between Bile Acids, All-Trans Retinoic Acid, and 1,25-Dihydroxy-Vitamin D₃ on Monocytic Differentiation and Myeloblastin Gene Down-Regulation in HL60 and THP-1 Human Leukemia Cells¹

The Hebrew University of Jerusalem, Faculty of Agriculture, Department of Animal Science, Rehovot 76100, Israel [A. Z.]; Institut Universitaire d’Hématologie, Hôpital Saint-Louis, 75475 Paris cedex 10, France [A. C., J. P. A.]; INSERM Unité 402, Faculté de Médecine Saint-Antoine, Université Paris VI, 75571 Paris Cedex 12, France [V. B.]; and INSERM Unité 482, Hôpital Saint-Antoine, 75571 Paris cedex 12, France [A. Z., C. G.]

Bile acids were shown previously to inhibit proliferation and to induce monocytic differentiation in HL60 human acute promyelocytic leukemia cells (A. Zimber et al., Int. J. Cancer, 59: 71–77, 1994). In this report, we hypothesized that bile acids may exert a positive cooperativity with two known inducers of leukemic cell differentiation, all-trans retinoic acid and 1,25(OH)₂-vitamin D₃. Our results provide evidence that bile acids induced the monocytic differentiation of HL60 and THP-1 human leukemia cells exposed to ineffective concentrations of these inducers. The protein kinase C (PKC) inhibitors H-7 (10 and 20 µM) and staurosporine (5 and 20 nM) modulated the effects of bile acids on HL60 cell differentiation. Most interestingly, bile acids are shown herein to down-regulate the expression of the serine protease myeloblastin gene involved in the differentiation of myeloid hematopoietic cells.

In agreement with the recent identification of nuclear receptors for bile acids, our data suggest that functional interactions between nuclear bile acid signaling pathways, PKC, and nuclear receptors for retinoic acid and vitamin D₃ are involved in the down-regulation of the myeloblastin gene and the induction of cell differentiation in human leukemic cells.

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