Open AccessKilling Effect of the Herpes Simplex Virus Thymidine Kinase/Ganciclovir Enzyme/Prodrug System on Human Nasopharyngeal Carcinoma Cells
Author(s) -
Yong Tang,
J Li,
Shufang Zhao,
J Liu
Publication year - 2007
Publication title -
journal of international medical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.421
H-Index - 57
eISSN - 1473-2300
pISSN - 0300-0605
DOI - 10.1177/147323000703500401
Subject(s) - thymidine kinase , ganciclovir , herpes simplex virus , suicide gene , prodrug , transfection , nasopharyngeal carcinoma , virology , genetic enhancement , cell culture , microbiology and biotechnology , cytotoxic t cell , biology , virus , medicine , human cytomegalovirus , gene , pharmacology , in vitro , radiation therapy , biochemistry , genetics
A promising new approach for the gene therapy of cancer is the introduction of the herpes simplex virus thymidine kinase (HSV tk) gene into tumour cells, where the HSV tk gene product converts the non-toxic prodrug ganciclovir (GCV) into its cytotoxic metabolite. We constructed a recombinant plasmid containing the HSV tk gene using standard molecular biology techniques in order to investigate whether the HSV tk/GCV enzyme/prodrug system could kill the human nasopharyngeal carcinoma cell line HNE-1. The recombinant plasmid pcDNA3.1(–) CMV.TK was transfected into the HNE-1 cells by electroporation. The expression of HSV tk by the transfected HNE-1/TK cells was confirmed by mRNA amplification and Western blotting. The growth of HNE-1/TK cells was inhibited by GCV in a dose-dependent manner. The HSV tk/GCV system also demonstrated a considerable bystander effect on co-cultured wild type HNE-1 cells. We conclude that the HSV tk/GCV system could be used as gene therapy for nasopharyngeal carcinoma.