Inhibition of human hepatocellular carcinoma cell proliferation by galactose receptor-mediated c-myc antisense oligonucleotide
- VernacularTitle:半乳糖受体介导的c-myc反义核酸对人肝癌细胞增殖的抑制作用
- Author:
Jianwei JIANG
;
Yuan ZHANG
- Publication Type:Journal Article
- Keywords:
Genes, c-myc;
Oligonucleotides, antisense;
Receptors, galactose;
Liver neoplasms;
Bel-7402 cells
- From:
Chinese Journal of Pathophysiology
2000;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To evaluate the inhibitory effect of galactose (Gal)-polyethyleneimine (PEI)-c-myc antisense oligodeoxynucleotide (ASODN) complex on proliferation of human hepatocellular carcinoma cells. METHODS: Human hepatocellular carcinoma cell line Bel-7402 was treated with Gal-PEI-ASODN complex. Cell proliferation was tested by trypan blue dye at different time points and with various concentrations of ASODN treatment. Cell morphology was observed under inverted microscope, cell hypodiploid percentage was analyzed by flow cytometry and cell ultrastructure was observed through electron microscopy. RESULTS: Compared with ASODN group (20 ?mol/L) from (0 h) to 96 h, Gal-PEI-ASODN complex (with ASODN 0.75 ?mol/L) significantly suppressed Bel-7402 cells proliferation, the ASODN concentration within Gal-PEI-ASODN complex and time course acquired were significantly lower and shorter, respectively. Incubated with pure ASODN at different concentrations for 72 hours, cell proliferation was inhibited and IC_(50) was 20.9 ?mol/L; while mediated with galactose receptor for 48 hours, ASODN significantly inhibited cell proliferation and IC_(50) was only 0.294 ?mol/L, the inhibitory efficacy of ASODN enhanced 70.9 folds. While Bel-7402 cells were incubated with Gal-PEI-ASODN complex for 48 hours, cell hypodiploid percentage was much higher than ASODN groups and cell apoptosis was seen under electron microscopy. CONCLUSIONS: Galactose receptor mediated ASODN delivery may significantly increase proliferation inhibition efficacy on Bel-7402 cells. [
