PURPOSE: Wnt signaling was demonstrated to be activated in chronic lymphocytic 
leukemia (CLL). It is thought to be responsible for the extended survival of CLL 
cells in vivo. Dickkopf1 (DKK1) is known to antagonize Wnt signaling by direct 
high-affinity binding to the extracellular domain of WNT coreceptor lipoprotein 
receptor-related protein 6 (LRP6). The purpose of this study was to investigate 
the effect of DKK1 in B-CLL cells in vitro.
METHODS: Expression of DKK1 was estimated by Western blot and real-time PCR. B 
cells from patients with CLL and healthy donors were incubated with recombinant 
DKK1. Survival was measured by flow cytometry. Primers for real-time PCR were 
designed for extracellular domain of LRP6, responsible for DKK1 binding, and the 
intracellular region, essential for inhibiting GSK3 β.
RESULTS: Healthy and CLL cells express equivalent mRNA levels of DKK1 and LRP6. 
After treatment of CLL cells with recombinant DKK1 (1 μg/mL) for 3 h, there was 
no change in the levels of phosphorylated β-catenin and total β-catenin. Healthy 
B cells proved to have significantly higher levels of extracellular, DKK1 
binding domain of LRP6. We estimated that in CLL cells every 6th LRP6 receptor 
is lacking the extracellular domain.
DISCUSSION: For the first time we show the expression of DKK1 in CLL cells. 
Unlike in similar tumors, the addition of DKK1 to culture of CLL cells does not 
inactivate WNT pathway. The reason for this could be the absence of the binding 
domain of LRP6. On the other hand, a truncated LRP6 without extracellular DKK1 
binding domain could lead to an uncontrollable activation of WNT signaling.