AIM:To study the interactions between human gastriccarcinoma cell(HGCC)and human vascular endothelialcell(HVEC),and if the expression of sphingosine kinase(SPK)gene was involved in these interactions.METHODS:The specific inhibitor to SPK,dimethylsphingosine(DMS),was added acting on HGCC andHVEC,then the cell proliferation was measured by MTT.The conditioned mediums(CMs)of HGCC and HVECwere prepared.TheCM of one kind of cell was added tothe other kind of cell,and the cell proliferation wasmeasured by MTT.After the action of CM,the cellularexpression of SPK gene in mRNA level was detectedwith in situ hybridization(ISH).RESULTS:DMS could almost completely inhibit theproliferation of HGCC and HVEC.The growth inhibitoryrates could amount to 97.21%,83.42 %,respectively(P<0.01).The CM of HGCC could stimulate the growthof HVEC(2.70±0.01,P<0.01)while the CM of HVEC couldinhibit the growth of HGCC(52.97±0.01%,P<0.01).There was no significant change in the mRNA level ofSPK gene in one kind of cell after the action of the CM ofthe other kind of cell.CONCLUSION:$PK plays a key role in regulating theproliferation of HGCC and HVEC.There exist complicatedinteractions between HGCC and HVEC.HGCC cansignificantly stimulate the growth of HVEC while HVECcan significantly inhibit the growth of HGCC.Theexpression of SPK gene is not involved in the interactions. AIM: To study the interactions between human gastric endothelial cells (HGCC) and human vascular endothelial cells (HVEC), and if the expression of sphingosine kinase (SPK) gene was involved in these interactions. METHODS: The specific inhibitor to SPK, dimethylsphingosine , was added acting on HGCC and HVC, then the cell proliferation was measured by MTT. The conditioned mediums (CMs) of HGCC and HVEC were prepared. TheCM of one kind of cell was added tothe other kind of cell, and the cell proliferation wasmeasured by MTT . After the action of CM, the cellularexpression of SPK gene in mRNA level was detected with in situ hybridization (ISH) .RESULTS: DMS could almost completely inhibit theproliferation of HGCC and HVEC.The growth inhibitoryrates could amount to 97.21%, 83.42%, respectively (P <0.01) .The CM of HGCC could stimulate the growth of HVEC (2.70 ± 0.01, P <0.01) while the CM of HVEC couldinhibit the growth of HGCC (52.97 ± 0.01%, P <0.01) in the mRNA level of SPK gene in one kind of c ell after the action of the CM of the other kind of cell.CONCLUSION: $ PK plays a key role in regulating theproliferation of HGCC and HVEC.There exist complicatedinteractions between HGCC and HVEC. HGCC cansignificantly stimulate the growth of HVEC while HVECcan significantly inhibit the growth of HGCC.Theexpression of SPK gene is not involved in the interactions.