Abstract

Human non-small cell lung cancer (NSCLC) cells were transfected with herpes simplex virus-thymidine kinase (HSV-tk) cDNA and the cells resistant to G418 were selected. Two clones were investigated based on their difference of the expression level of HSV-tk and investigated for their sensitivity toward exogenous ganciclovir (GCV). The apoptosis from cell susceptibility to (ley and the bystander effect is dependent on the level of HSV-tk followed by activation of cell cycle modulators and tumor suppressor p53. The study provided a model for better understanding of gene therapy in cancer cells that helps the in vivo work.

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