Influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside to HL-60 cell.
- Author:
Li WEI
1
;
Pei-Yan KONG
;
Xing-Hua CHEN
;
Xian-Gui PENG
;
Dong-Feng ZENG
;
Cheng CHANG
;
Wen-Bo YANG
;
Hong LIU
;
Lin LIU
;
Qing-Yu WANG
;
Yi ZHANG
Author Information
1. Department of Hematology, Xinqiao Hospital, The Third Military Medical University, Chongqing 400037, China.
- Publication Type:Journal Article
- MeSH:
Antibodies, Monoclonal;
pharmacology;
Antimetabolites, Antineoplastic;
pharmacology;
Cell Line, Tumor;
Cell Survival;
drug effects;
Cytarabine;
pharmacology;
Dose-Response Relationship, Drug;
Drug Synergism;
HL-60 Cells;
Humans;
Receptors, CXCR4;
immunology
- From:
Journal of Experimental Hematology
2005;13(2):269-273
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside (Ara C) to HL-60 cell, and to assess its therapeutic value in marrow residual disease. HL-60 cells were cultured and co-cultured with leukemic stromal cells, and SDF-1 activity was inhibited with 10 microg/ml 12G5, then, killing effects of Ara C on HL-60 cells were investigated by MTT and morphology assay. Curves by MTT assay revealed that in the test group of 20 microg/ml Ara C, A(540) values decreased slowly but straightly, however, in control group A(540) values decreased markedly for the first two days, and increased from day 3 or 4. In the test group of 40 microg/ml Ara C, although increasing at constricted range of 7 - 9 days, A(540) values decreased in whole observing period of 12 days, while in control group A(540) values decreased markedly at day 0-3, and increased from day 4. Furthermore, two curves go across each other at day 5, and continue the increasing tendency. Morphology results showed that in both treated groups, the number of HL-60 cell decreased markedly and increased gradually in control group, but just contrary to test group. It is concluded that 12G5 may weaken the killing effect of Ara C on HL60 cell in earlier period, but reinforce the total killing effect and delay the occurrence of drug resistance simultaneously. Thus 12G5 has the therapeutic potential on marrow residual disease.
