Objective: To study the changes in the expressions of beta1-integrin receptor (CD29) and focal adhesion kinase (FAK) during the deterioration of chronic myeloid leukemia (CML), thereby explore the potential mechanism of interferon (IFN)-alpha in the treatment of CML through testing the quantitative changes of FAK.
Methods: Bone marrow mononuclear cells were tested for CD34, CD29 and FAK monoclonal antibody by flow cytometry in CML patients of the chronic phase and blast crisis and in normal subjects. In the presence or absence of IFN-alpha, the bone marrow mononuclear cells from CML patients of chronic phase and normal subjects were cultured for 48 h to determine the content of FAK in the cells with Western blotting.
Results: CD 29 expression on the surface of CD34+ cells scarcely differ between normal subjects and CML patients of chronic-phase, but the intracellular content of FAK was lower in the latter. The expression of beta1-integrin receptor on the surface of hematopoietic cells in CML patients with blast crisis was significantly higher than that in chronic-phase CML patients, but the intracellular FAK in the former patients was lower. No difference of FAK content was observed in normal mononuclear cells before and after IFN-alpha treatment, while the treatment increased FAK content in the mononuclear cells in chronic phase CML patients.
Conclusion: The changes in the expressions of beta1-integrin receptor and FAK may play important roles during CML deterioration, and IFN-alpha may function to repair the defect in the beta1-integrin receptor pathway by restoring the cellular content of FAK.