We evaluated the relationship between cellular gap junction and bystander effect in gastric cancer SCG7901 cell killing by adenovirus-mediated KDR-CDglyTK system. SCG7901 and HeLa cells were transfected (MOI-100) with recombinant adenovirus carrying fusion gene. Transfection efficiency/fusion gene mRNA expression were determined; intercellular communications in the presence of apigenin were measured by fluorescence recovery after photobleaching (FRAP). Transfected/non-transfected cells were mixed at 5:95/10:90% ratios, respectively, incubated for 24 h with/without apigenin, and for 72 h with GCV and 5-FU. Cell survival was determined by MTT method. The transfected SCG7901/HeLa cells expressed GFP. Fluorescence intensity in SCG7901 cells decreased after photobleaching but recovered over time. Fluorescence intensity in HeLa cells also decreased after photobleaching with no recovery. Following apigenin treatment, fluorescence intensity differed between SCG7901 and HeLa cells. Survival rates of SCG7901 cells differed among prodrug, apigenin, and prodrug + apigenin groups compared with controls, but no significant difference was observed for HeLa cells. We concluded that the intercellular communication in SCG7901 cells related with the gap junctions, while there was no such communication in HeLa cells. The bystander killing effect related with the intercellular gap junctions and was increased by apigenin with no such effect seen in HeLa cells.