Effects of dexamethasone on Flt3 receptor expression and proliferation induced by recombinant human Flt3 ligand in malignant hematopoietic cells
Abstract
Aim: To investigate the effect of dexamethasone (DXM) on the expression of Flt3 receptor and the proliferation mediated by recombinant human Flt3 ligand (rhFL) in leukemia cells.
Methods: Eighteen malignant hematopoietic cell lines and 10 leukemia blasts from leukemia patients were examined by flow cytometry for the expression of Flt3 receptor before and after incubation with DXM 0.1 micromol/L for 24 h. The effect of DXM on the proliferation of malignant hematopoietic cells was measured by MTT assay.
Results: (1) Expression of the Flt3 receptor in malignant hematopoietic cell lines and leukemia blasts was widespread and extremely heterogeneous; (2) The presence of receptor on the surface of malignant hematopoietic cell didn't necessarily imply a significant ligand-induced response, at least in terms of proliferation. Conversely, some Flt3 receptor-negative malignant hematopoietic cells responded to rhFL; (3) DXM down-regulated the expression of Flt3 receptor and inhibited the proliferation induced by rhFL in some malignant hematopoietic cell lines and fresh leukemia cells.
Conclusion: DXM may down-regulate the expression of Flt3 receptor on the surface of malignant hematopoietic cells and inhibit the proliferation induced by rhFL. A combination of rhFL and DXM may serve to control hematopoietic defects in malignant hematopoietic diseases.
Keywords:
Methods: Eighteen malignant hematopoietic cell lines and 10 leukemia blasts from leukemia patients were examined by flow cytometry for the expression of Flt3 receptor before and after incubation with DXM 0.1 micromol/L for 24 h. The effect of DXM on the proliferation of malignant hematopoietic cells was measured by MTT assay.
Results: (1) Expression of the Flt3 receptor in malignant hematopoietic cell lines and leukemia blasts was widespread and extremely heterogeneous; (2) The presence of receptor on the surface of malignant hematopoietic cell didn't necessarily imply a significant ligand-induced response, at least in terms of proliferation. Conversely, some Flt3 receptor-negative malignant hematopoietic cells responded to rhFL; (3) DXM down-regulated the expression of Flt3 receptor and inhibited the proliferation induced by rhFL in some malignant hematopoietic cell lines and fresh leukemia cells.
Conclusion: DXM may down-regulate the expression of Flt3 receptor on the surface of malignant hematopoietic cells and inhibit the proliferation induced by rhFL. A combination of rhFL and DXM may serve to control hematopoietic defects in malignant hematopoietic diseases.