<正>Objective:To investigate the expression of CXCR

on HL-60 cell line and the proliferation

apoptosis of HL-60 cell line cocultured with bone marrow stromal cells

so as to assess the possibility of 12G5. an anti-CXCR4 monoclonal antibody

in eradicating the minimal residual disease. Methods:The activity of SDF-1 was inhibited by 10μg/ml 12G5. After treatment with 12G5. the status of adhesion was observed

and the adhesion rates

apoptosis and cell cycles were detected after 24 h of treatment. Cell growth rates were measured by trypan blue exclusion. Cell growth curve was plotted

and the expression of PCNA and apoptosis related protein including PCNA

Bcl-2 and Fas were detected with immunohis-tochemical technique. Results :（1） There was middling degree expression of CXCR4 on HL-60 membrane. From 0 h to 6 h

as the time of 12G5 incubation along

the expression of CXCR4 decreased gradually. （2） After treatment for 24 h

the adhesion rates in the experiment group and the control were （39. 4±7. 9）% and （51. 4±5. 9）%

respectively. （3）After treatment for 24 h

the percentage of HL-60 cells in G0/G1 phase were （55. 21±4. 9）%

and that in S phase and G2/M phase were （30. 40±4. 1）% and （14. 39±5.2）%

respectively

with the corresponding proportions being （44. 67±2. 2） %

（45. 30±3. 7）% . and （10. 03±2. 6）% in the control. （4） The percentage of apoptotic HL-60 cells was （8. 95±1. 7）% in the experiment group

compared to （3. 97±2. 4）% in the control. （5）The survival rates of HL-60 cells decreased markedly at 48 h to 96 h

and the proliferation slowed down at this time duration. （6）The expression of PCNA and Bcl-2 down-regulated significantly

but the Fas protein expression was up-regulated. Conclusion :12G5 could inhibit the capability of adhesion and proliferation of HL-60 cells and it can induce more cells to enter G0/G1 phase and promote apoptosis. It may be helpful by inhibiting the bioactivity of SDF-1 with 12G5 in the therapy of marrow residual disease.