Citation

Yang C, Deng Z, Liu Y, Liu J, Cao Y. Zhonghua Gan Zang Bing Za Zhi 2008; (12): 509-513.

Copyright

(Copyright © 2008, Chongqing yi ke da xue di er lin chuang xue yuan bing du xing gan yan yan jiu suo)

DOI

unavailable

PMID

unavailable

Abstract

OBJECTIVETo observe the targeted therapeutic effects of plasmid AF-pGL3-hTERT-TK on HepG2 cells.

METHODSHepG2 cells were cultured and pGL3-hTERT-TK and AF-liposome were constructed. HepG2 and L02 cells were transfected with AF-pGL3-hTERT-TK. The growth, apoptosis of the cells and the bystander effects were studied using liquid scintillation analysis and tunnel and flow cytometry.

RESULTSAfter the suicide gene was inserted into the downstream of hTERT, TK was effectively driven by the hTERT promoter, making the TK highly expressed in the HepG2 cells. The AF made the therapeutic gene enter the HepG2 cells more easily by recognizing and combining the ASGPR receptor protein on the HepG2 cell surfaces and induced their apoptosis and suicide with bystander effect. The apoptosis rate was 85%+/-3% in the HepG2 cells whereas in the normal L02 hepatic cells it was 16%+/-2%.

CONCLUSIONAF-pGL3-hTERT-TK can target and attack HepG2 cells and has almost no influence on normal L02 hepatic cells. AF-pGL3-hTERT-TK has a potential in the treatment of hepatocellular carcinomas.

Language: zh