Arsenic trioxide induced apoptosis in retinoblastoma cells in vitro and its possible mechanism.
- Author:
Yun LI
1
;
Luo-Sheng TANG
;
Hong-Wei SHEN
Author Information
1. Department of Ophthalmology, Second Xiangya Hospital, Central South University, Changsha 410011, China. yunli0904@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Arsenic Trioxide;
Arsenicals;
pharmacology;
Caspase 3;
biosynthesis;
Humans;
Oxides;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
Retinal Neoplasms;
pathology;
Retinoblastoma;
pathology;
Tumor Cells, Cultured;
bcl-2-Associated X Protein;
biosynthesis
- From:
Journal of Central South University(Medical Sciences)
2008;33(6):476-480
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effect of arsenic trioxide on the apoptosis of retinoblastoma cell line HXO-RB(44) and the possible mechanism.
METHODS:The effect of arsenic trioxide on the proliferation of retinoblastoma cell line HXO-RB(44) was observed by MTT colorimetric assay; the apoptosis of the HXO-RB(44) was examined by AO/EB staining and flow cytometry analysis (Annexin V+ PI staining); caspase-3 activity and bcl-2/bax expression in the HXO-RB(44) were detected by cpp32 colorimetric assay kit and Western blot.
RESULTS:Arsenic trioxide inhibited the proliferation of HXO-RB(44) cell in dose and duration-dependent manner in vitro; arsenic trioxide significantly increased the apoptosis in HXO-RB(44) cells. The activation of caspase-3 was increased, and the rate of bcl-2/bax was down-regulated in the HXO-RB(44) cells processed with arsenic trioxide.
CONCLUSION:Arsenic trioxide can inhibit the proliferation of retinoblastoma cell HXO-RB(44) in vitro by apoptosis induction. The apoptosis induction is possibly related to the caspase-3 activation and bcl-2/bax down-regulation.
