Biological response of B-cell lymphoma cells in vitro to 131I-rituximab.
- Author:
Li WEI
1
;
Rong-cheng LUO
;
Jun-yi ZHANG
;
Xiao YAN
;
Yong-xin FANG
;
Li-hua FEI
Author Information
- Publication Type:Journal Article
- MeSH: Antibodies, Monoclonal; immunology; pharmacology; Antibodies, Monoclonal, Murine-Derived; Antigens, CD20; immunology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Flow Cytometry; Humans; Iodine Radioisotopes; Lymphoma, B-Cell; immunology; pathology; physiopathology; Radioimmunotherapy
- From: Journal of Southern Medical University 2006;26(2):211-213
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the biological response of B-cell lymphoma cells positive for CD20 expression to (131)I-labeled rituximab.
METHODSAnti-CD20 monoclonal antibody rituximab was labeled with (131)I by means of IODO-GEN method, and its effects on apoptosis of Raji cells were determined by Annexin-V/PI double-labeled cytometry. Its effects on the cell cycles was evaluated by cytometry with PI staining.
RESULTSThe cell apoptosis rate measured by Annexin v-FITC/PI was 51.99% in (131)I-rituximab group, significantly higher than that in (131)I group, rituximab group and control group (42.71%, 29.42% and 26.17%, respectively, P<;0.05). The apoptosis rate by flow cytometry with PI staining was 4.32% in (131)I-rituximab group, also significantly higher than that in the other 3 groups (1.47%, 1.39% and 0.37%, respectively, P<0.05). Cell cycle alteration of Raji cells occurred in (131)I-rituximab group, and the majority of cells were arrested at G(1)/G(2) stage.
CONCLUSION(131)I-rituximab can regulate the cell cycle of Raji cells and induce their apoptosis to inhibit their proliferation.
