Proliferation regulation effect of cyclin G1 antisense oligodeoxy-nucleotides with liposomal transfection on HL-60 cell.
- Author:
Jin-Song JIA
1
;
Shi-Rong XU
;
Cong-Rong JIA
;
Jie MA
;
Sen HA
;
Yin-Rong YAO
;
Yi WANG
;
Cui-Ying SHI
Author Information
1. Department of Hematology, The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China. jiajsong@mail.com
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Division;
drug effects;
Cyclin G;
Cyclin G1;
Cyclins;
antagonists & inhibitors;
genetics;
Flow Cytometry;
HL-60 Cells;
cytology;
drug effects;
Humans;
Liposomes;
Microscopy, Electron;
Oligonucleotides, Antisense;
pharmacology;
Transfection
- From:
Journal of Experimental Hematology
2004;12(1):48-54
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of cyclin G1 antisense oligodeoxynucleotide (ASON) with liposomal transfection on mediating proliferation of HL-60 cell, the cyclin G1 ASON with liposomal transfection was used in vitro in co-culture with HL-60 cell, the protein and mRNA expression levels of cyclin G1 were measured by immunocytochemistry assay and RT-PCR. The cell apoptosis was detected by electron microscopy, in situ cell apoptosis detection kit (POD), DNA gel electrophoresis and flow cytometry (FCM). The results showed that in the cyclin G1 ASON group the protein and mRNA expression of cyclin G1 were significantly inhibited as compared with sense oligodeoxynucleotide (SON) group and blank group. When the ASON concentration increased, the proliferation ratio of HL-60 cell and CFU of HL-60 were also significantly inhibited. There was apoptosis of HL-60 cell. In conclusion, cyclin G1 ASON can specifically inhibit its protein and mRNA expression levels as well as the HL-60 cell proliferations and can accelerate the apoptosis of leukemia cells with concentration-dependent effect of ASON.