Replication-incompetent Adenovirus Vector-mediated MDA-7/IL-24 Selectively Induces Growth Suppression and Apoptosis of Hepatoma Cell Line SMMC-7721
- Author:
WANG CONGJUN
1
;
XUE XINBO
;
YI JILIN
;
WU ZAIDE
;
CHEN KUN
;
ZHENG JIANWEI
;
JI WENWEI
;
YU YUAN
Author Information
1. 华中科技大学同济医学院附属同济医院
- Keywords:
cancer gene therapy;
hepatocellular carcinoma;
apoptosis;
growth suppression;
MDA-7/IL-24
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2008;28(1):80-83
- CountryChina
- Language:Chinese
-
Abstract:
In order to investigate the effect of replication-incompetent adenovirus vector expressing MDA-7/IL-24 on tumor growth and apoptosis of human hepatocellular carcinoma (HCC) cell line SMMC-7721 and normal liver cell line L02, the recombinant replication-incompetent Ad.mda-7 virus vector was constructed and infected into the HCC cell line SMMC-7721 and normal liver cell line L02. RT-PCR was performed to examine the expression of MDA-7 mRNA. The concentrations of MDA-7/IL-4 in culture supernatants were determined by using ELISA. MTT and Hoechst staining assay were applied to observe the inhibitory and killing effects of MDA-7 on the HCC cells. By using flow cytometry, the apoptosis, cell cycle and proliferation of SMMC-7721 and L02 cells were meas- ured. The results showed recombinant replication-incompetent virus expressing MDA-7/IL-24 was constructed successfully, and RT-PCR revealed that it could mediate the high expression of the ex- ogenous gene MDA-7/IL-24 in SMMC-7721 and L02 cells. The expression of MDA-7/IL24 proteins in the culture supernatant was detectable by ELISA. Ad.mda-7 infection induced apoptosis and growth suppression in SMMC-7721 cells and an increased percentage of HCC cells in the G2/M phase of the cell cycle, but not in L02 cells. It was concluded that mda-7/IL-24 gene, mediated with replication-incompetent adenovirus vector, could selectively induce growth suppression and apoptosis in HCC cell line SMMC-7721 but without any toxic side-effect on normal liver line L02.
