Laminin promotes differentiation of NB4 promyelocytic leukemia cells with all-trans retinoic acid

HE PROMYELOCYTIC leukemia cell line, NB4, was T derived from a patient with acute promyelocytic leukemial and carries the t(15;17) translocation resulting in the joining of the PML oncogene to the gene encoding the retinoic acid receptor a (RARa). PML is part of a macromolecular nuclear organelle' believed to function as a promoterspecific transcriptional repre~sor.~ The PML-RARa fusion protein acts as a dominant negative inhibitor of PML and disrupts the normal nuclear structures that contain PML.'-4 Treatment with all-trans retinoic acid (ATRA) results in commitment and maturation along the myeloid lineage in nearly all patients who carry molecular evidence of this transl~cation.~-* Moreover, RA restores normal PML distribution and function to native cells from patients with acute promyelocytic leukemia or to the cell line, NB4.24 Early in vitro studies suggested that retinoids could have a therapeutic benefit in leukemia. For example, RA was shown to inhibit growth of several myeloid leukemia cell lines, including KG-1 acute myeloblastic leukemia and HL60 acute promyelocytic leukemia cell lines as well as the in vitro clonal growth of leukemia cells from patients with acute myeloid leukemia (AML).9 Further investigation showed that RA induced morphologic changes consistent with terminal maturation of both HL-60 cells" and cells derived from some patients with AML." ATRA binds to nuclear RAR.'' These receptors form heterodimers with the retinoic X receptors (RXR), resulting in the RAR/RxR dimer capable of transactivating responsive genes. Synthetic ligands have been developed that can bind selectively to the RAFURXR heterodimer or the RxRmxR homodimer, enabling the receptors critical for a particular function to be identified. Using these ligands with myeloid cell lines, it was determined that the differentiating effects of the retinoids were mediated through the RAR/RXR heterodimer~.'~ Two NB4 cell lines have been isolated from a patient in relapse that do not mature in response to ATRA.'4*'5 These have been designated NB4-RA' R1 and R2. The R1 resistant subline upregulates CDI lc/CD18 in response to ATRA and does exhibit enhanced growth in low-dose ATRA (15 to 150 nmom), although maturation is not achieved. The R2resistant subline exhibits none of these responses to Am. Elevation of adenosine-3',5'-cyclic monophosphate (CAMP)

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