Abstract
Among gene therapy strategies elaborated to kill cancer cells, one uses the CodA gene, coding for cytosine deaminase (CD) that converts 5-fluorocytosine (5-FC) into toxic 5-fluorouracil (5-FU). To enhance 5-FC metabolic activation, we prepared a vector carrying CodA and upp (uracil phosphoribosyl transferase) genes which rendered HeLa cells sensitive to 5-FC and enhanced a bystander effect not mediated by gap junctions. However, 1% CD +–UPP + cells were able to kill 40% of the cell population if the cells were communicating. This suggests that, at very low percentages of CD +–UPP + cells, CodA and upp induce a bystander effect through gap junction-dependent mechanisms.
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