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AIM:To elucidate whether human primary gastric cancerand gastric mucosa epithelial cells in vitro can grownormally in a rnethionine(Met)depleted environment,i.e.Met-dependence,and whether Met-depleting status canenhance the killing effect of chemotherapy on gastric cancercells.METHODS:Fresh human gastric cancer and mucosal tissueswere managed to form monocellular suspensions,whichware then cultured in the Met-free but homocysteine-containing(Met~-Hcy~+)medium,with differentchemotherapeutic drugs,The proliferation of the cells wasexamined by cell counter,flow cytometry(FCM)andmicrocytotoxicity assay(IVITT).RESULTS:The growth of human primary gastric cancer cellsin Met~-Hcy~+was suppressed,manifested by the decrease oftotal cell counts[1.46±0.42(×10~9·L~(-1))in Met~-Hcy~+vs.64±0.44(×10~9·L~(-1))in Met~+Hcy~-,P<0.01],the decline inthe percentage of G_0G_1 phase cells(0.69±0.24 in Met~-Hcy~+vs 0.80±0.18 in Met~+Hcy~-,P<0.01)and the increase of Scells(0.24±0.20inMet~-Hcy~+vs 0.17±0.16 in Met~+Hcy~-,P<0.01);howaver,gastric mucosal cells grew normally.IfMet~-Hcy~+medium was used in combination withchemotherapeutic drugs,the number of surviving gastriccancer cells dropped significantly.CONCLUSION: Human primary gastric cancer cells in vitro are Met dependent; however, gastric mucosal cells have not shown the same characteristics. Met Hcy* environment may strengthen the killing effect of chemotherapy on human primary gastric cancer cells.
AIM: To elucidate whether human primary gastric cancer and gastric mucosa epithelial cells in vitro can grown normally in a rnethionine (Met) depleted environment, ie Met-dependence, and whether Met-depleting status canenhance the killing effect of chemotherapy on gastric cancer cells. METHODS: Fresh human gastric cancer and mucosal tissueswere managed to form monocellular suspensions, which were then cultured in the Met-free but homocysteine-containing (Met ~ -Hcy ~ +) medium, with different chemotherapeutic drugs, The proliferation of the cells wasexamined by cell counter, flow cytometry (FCM) andmicrocytotoxicity assay (IVITT) .RESULTS: The growth of human primary gastric cancer cellsin Met ~ -Hcy ~ + was suppressed, manifested by the decrease of total cell counts [1.46 ± 0.42 (× 10 ~ 9 · L -1 ) in Met ~ -Hcy ~ + vs.64 ± 0.44 (× 10 ~ 9 · L -1) in Met ~ + Hcy ~ -, P <0.01], the decline inthe percentage of G_0G_1phase cells ± 0.24 in Met ~ -Hcy ~ + vs 0.80 ± 0.18 in Met ~ + Hcy ~ -, P <0.01) and the increase of Scells (0.24 ± 0.20 inMet ~ -Hcy ~ + vs 0.17 ± 0.16 in Met ~ + Hcy ~ -, P <0.01); howaver, gastric mucosal cells grew normally.IfMet ~ -Hcy ~ + medium was used in combination with chemotherapeutic drugs, the number of surviving gastriccancer cells dropped significantly.CONCLUSION: Human primary gastric cancer cells in vitro are Met dependent; however, gastric mucosal cells have not shown the same characteristics. Met Hcy * environment may strengthen the killing effect of chemotherapy on human primary gastric cancer cells.