Cytokine-induced killer cells induce apoptosis of K562 cells expressed bcr-abl.
- Author:
Xi-Nan CEN
1
;
Ping ZHU
;
Yong-Jin SHI
;
Ya-Li REN
;
Ming-Xin MA
;
Ji-Ren YU
Author Information
1. Department of Hematology, The First Hospital, Peking University, Beijing 100034, China. cenxn@hotmail.com
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents, Phytogenic;
pharmacology;
Apoptosis;
drug effects;
immunology;
Camptothecin;
pharmacology;
Coculture Techniques;
Cytotoxicity, Immunologic;
Etoposide;
pharmacology;
Flow Cytometry;
Fusion Proteins, bcr-abl;
genetics;
Gene Expression Regulation, Neoplastic;
Humans;
K562 Cells;
drug effects;
immunology;
metabolism;
Killer Cells, Lymphokine-Activated;
cytology;
immunology
- From:
Journal of Experimental Hematology
2002;10(3):201-204
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate whether cytokine-induced killer (CIK) cells can induce apoptosis of bcr-abl(+) K562 cells, apoptosis of K562 cells and CEM cells induced by CIK cells, etoposide or camptothecin was detected with flow cytometry DNA assay. RT-PCR showed that K562 cells expressed the bcr-abl fusion gene, K 562 cells, K562 cells/etoposide or K562 cells/camptothecin groups showed no sub-G(1) peak. K562 cells/CIK cells group showed sub-G(1) peak (38.1%). CEM cells showed no sub-G(1) peak. CEM cells/camptothecin or CEM cells/etoposide groups showed sub-G(1) peak (23.5% or 32.3% respectively). CEM cells/CIK cells group showed sub-G(1) peak (45.4%). Etoposide or camptothecin did not induce apoptosis of K562 cells. CIK cells induce apoptosis of K562 cells. Bcr-abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells. This property may support the observed adoptive immunologic effect of allogeneic bone marrow transplantation and donor lymphocyte transfusions of CML case relapsing after allogeneic bone marrow transplantation.
