Loss of CDK2 induces the differentiation of AML cells. (A) The silencing efficiency of different shRNA (#1, #2, and #3) against CDK2 in HL60 cells. The protein levels of CDK2 were measured by western blotting. (B-E) Cell differentiation analysis of HL60 cells infected with lentivirus-shCDK2s for the indicated times. (B) Cell proliferation assay. (C) CD11b expression. (D) NBT-reducing activity. (E) Cell morphological analysis after Wright-Giemsa staining. (F) The protein expression levels of CDK1 and CDK2 in HL60 cells infected with lentivirus-shCDK2 or lentivirus-shCDK1 for 72 hours. (G) CD11b expression in HL60 cells transduced with different lentiviruses for the indicated times. (H) Western blotting analysis of CDK2/1 and PU.1 expression in HL60 cells transduced with different lentiviruses for the indicated times. (I) Bacterial killing ability of THP-1, NB4, and U937 cells infected with different shRNA lentivirus (shCDK2 #2, shCDK4 #1, or shCDK6 #2) for 7 days. Clearance efficiency was determined from the numbers of viable bacteria recovered from the intracellular compartment after infection. S aureus were used to infect AML cells. (J) The differentiation of primary AML cells was assessed by CD11b expression. Primary AML samples collected from the peripheral blood of patients at diagnosis were infected with shCDK2 #2 lentivirus for 9 days. (A-D,G,I) *P < .05; **P < .01; ***P < .001 vs scramble. Data are shown as mean ± SD, n = 3. Other data are representative of at least 3 individual experiments; 1 representative image is shown. GAPDH, glyceraldehyde-3-phosphate dehydrogenase.