Growth inhibition of cancer cells by co-transfection of diphtheria toxin A-chain gene plasmid with bovine leukemia virus-tax expression vector

We constructed a plasmid containing bovine leukemia virus (BLV)-tax gene dr iven by SR alpha promoter, designated as pME-BLVtax, to activate the promot er of the long terminal repeat (LTR) of BLV in various tumor cells. Activat ion of the promoter of BLV-LTR by pME-BLVtax was confirmed by luciferase as say, When the cells, such as COS-1, C8, and KU-1, were transfected with a p lasmid pBLV-LUC1, which contained the luciferase gene under the control of BLV-LTR, and pME-BLVtax, luciferase was expressed in these cells, whereas n o luciferase gene expression was observed when only pBLV-LUC1 was introduce d into the cells, Activation of the BLV-LTR promoter was regulated by pME-B LVtax and 0.5 mug of pME-BLVtax was sufficient for the expression of the ge ne 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 con trol of BLV-LTR (pLTR-DT) to various tumor cell lines, KU-1, C8, COS-1, BL2 M3, and HeLa cells. The transfection was carried out with cationic liposome s, In this experiment, co-transfection of pLTR-DT with pME-BLVtax exerted s elective growth inhibitory effects on the tumor cell lines. Moreover, three co-introductions of pLTR-DT with pME-BLVtax into the cell lines resulted i n 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 t reatment of tumor cells.