Synergistic effect of Apo2L and chemotherapeutic agents on leukemia cells.
- Author:
Ling-ling WANG
1
;
Mao-hong ZHANG
;
Cong-gao XU
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis Regulatory Proteins; Cytarabine; pharmacology; Drug Synergism; Etoposide; pharmacology; Female; HL-60 Cells; Humans; Leukemia; drug therapy; Male; Membrane Glycoproteins; pharmacology; Receptors, TNF-Related Apoptosis-Inducing Ligand; Receptors, Tumor Necrosis Factor; genetics; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Journal of Hematology 2003;24(11):593-595
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore if the antileukemic drugs Vp16 or Ara-C are able to upregulate DR5 gene expression and enhance Apo2L-induced apoptosis of HL-60 cells.
METHODSCell apoptosis was determined by flow cytometry after annexin V/PI staining, the effect of Apo2L on fresh leukemia cells by MTT reduction assay, the expression of DR5 gene in HL-60 cells by semi-quantitative RT-PCR.
RESULTS1. Apo2L induced apoptosis of HL-60 cells in a dose-dependent manner. 2. Apo2L inhibited the proliferation of fresh leukemia cells, but there was difference among different subtypes. 3. Vp16 or Ara-C upregulated DR5 gene expression and augmented Apo2L-induced apoptosis in HL-60 cells.
CONCLUSIONApo2L could induce apoptosis of HL-60 cells and inhibit the proliferation of fresh leukemia cells. Ara-C or Vp16 upregulated DR5 gene expression and increased the sensitivity of HL-60 to Apo2L-induced cytotoxicity. Apo2L might be a promising antileukemic agent for the treatment of leukemia.
