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Growth Inhibition of Cancer Cells by Co‐Transfection of Diphtheria Toxin A‐Chain Gene Plasmid with Bovine Leukemia Virus‐Tax Expression Vector
Author(s) -
Watarai Shinobu,
Aida Yoko,
Tajima Shigeru,
Kakidani Hitoshi,
Onuma Misao,
Kodama Hiroshi
Publication year - 2001
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2001.tb02644.x
Subject(s) - transfection , luciferase , microbiology and biotechnology , biology , bovine leukemia virus , diphtheria toxin , cell culture , plasmid , expression vector , cationic liposome , hela , reporter gene , genetic enhancement , gene expression , virus , gene , virology , biochemistry , toxin , recombinant dna , genetics
We constructed a plasmid containing bovine leukemia virus (BLV)‐tax gene driven by SRα promoter, designated as pME‐BLVtax, to activate the promoter of the long terminal repeat (LTR) of BLV in various tumor cells. Activation of the promoter of BLV‐LTR by pME‐BLVtax was confirmed by luciferase assay. When the cells, such as COS‐1, C8, and KU‐1, were transfected with a plasmid pBLV‐LUC1, which contained the luciferase gene under the control of BLV‐LTR, and pME‐BLVtax, luciferase was expressed in these cells, whereas no luciferase gene expression was observed when only pBLV‐LUC1 was introduced into the cells. Activation of the BLV‐LTR promoter was regulated by pME‐BLVtax and 0.5 μg of pME‐BLVtax was sufficient for the expression of the gene under the control of BLV‐LTR. Furthermore, pME‐BLVtax was used to direct the cell expression of the gene for diphtheria toxin A‐chain under the control of BLV‐LTR (pLTR‐DT) to various tumor cell lines, KU‐1, C8, COS‐1, BL2M3, and HeLa cells. The transfection was carried out with cationic liposomes. In this experiment, co‐transfection of pLTR‐DT with pME‐BLVtax exerted selective growth inhibitory effects on the tumor cell lines. Moreover, three co‐introductions of pLTR‐DT with pME‐BLVtax into the cell lines resulted in significant inhibition of the cell growth. This result suggests that the delivery of the pLTR‐DT and pME‐BLVtax genes into tumor cells by the use of cationic liposomes may be potentially useful as a novel approach for the treatment of tumor cells.