Abstract: | OBJECTIVE: To investigate the cell cytotoxicity induced by the antineoplastic parvovirus H‐1 in gastric carcinoma cells. METHODS: The cytotoxicity of the H‐1 virus in the gastric cancer cell strain HGC27 was measured by MTT test and FACS analysis. The mRNA expressions of genes related to the mitogen‐activated protein kinase (MAPK) signaling transduction pathway were measured by RT‐PCR in HGC27 cells infected by the H‐1 virus. RESULTS: HGC27 cells were sensitive to the cytotoxicity of the H‐1 virus, although the cell cycle distribution was not significantly changed. The RT‐PCR results showed that 48 h after H‐1 virus infection of HGC27 cells the expression of creb was increased and that of erk1, stat2, p38‐γ, mek2, B‐raf and mtk1 was remarkably decreased. However, the expression of each of jnk2, ets and erk2 was unchanged. CONCLUSIONS: The mechanism of the cytotoxic effect of parvovirus H‐1 in HGC27 cells might be interference with specific cellular signaling transduction pathways, which would induce cell death. A modified and reconstructed parvovirus H‐1 could be a very useful tool for antitumor biochemical therapy. |