Mechanism of arsenic trioxide-induced apoptosis in hepatic blastoma cells HepG2.
- Author:
Ding YU
1
;
Zi-hui WANG
;
Li-yuan ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Apoptosis; drug effects; Arsenicals; pharmacology; Hep G2 Cells; Hepatoblastoma; chemistry; drug therapy; pathology; Humans; Liver Neoplasms; chemistry; drug therapy; pathology; Nuclear Proteins; analysis; Oxides; pharmacology; Promyelocytic Leukemia Protein; Transcription Factors; analysis; Tumor Suppressor Proteins; analysis
- From: Chinese Journal of Oncology 2003;25(2):120-123
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of arsenic trioxide (As(2)O(3)) induced apoptosis in hepatic blastoma cells HepG2 and its effects on cell nuclear matrix related protein promyelocytic leukaemia (PML).
METHODSHepG2 cells were cultured in MEM medium and treated with different concentrations of As(2)O(3) for either 24 h or 96 h. In situ terminal deoxynucleotidyl transferase (TdT) labeling (TUNEL) and DNA ladder were applied to detect apoptosis. Confocal microscopy and western blot were performed to observe the expression of PML.
RESULTSTUNEL positive apoptotic cells and DNA ladder could be detected in As(2)O(3) treated groups. The expression of PML decreased in HepG2 cells with 2 micro mol/L As(2)O(3), and micropunctates characteristic of PML protein in HepG2 cell nuclei almost disappeared after the treatment of 5 micro mol/L As(2)O(3).
CONCLUSIONAs(2)O(3) induces HepG2 tumor cell apoptosis in a time- and concentration-dependent manner. As(2)O(3) may degradate the PML protein in HepG2 cell nuclei. The decreased expression of PML is closely correlated with apoptosis. Nuclear matrix associated protein PML could be the target of As(2)O(3) therapy.
