目的 观察共轭亚油酸(conjugated linoleic acid．CLA)对黑色素瘤细胞B16-MB黏附和运动能力的影响，探讨CLA预防肿瘤转移的可能作用途径。方法 采用鼠黑色素瘤B16-MB商转移细胞系，用0.25、50、100、200pmol/L CLA处理后，分别用黏附试验、随机运动试验．Transwell趋化运动模型束研究CLA对细胞的黏附和运动能力的影响。结果 经CLA处理后，Bl6-MB向细胞外基质成分的黏附能力降低，同时随机运动能力降低，但趋向运动能力未发现变化。结论 CIA可能通垃抑制肿瘤细胞的粘附和运动能力来发挥预防肿瘤转移的作用。

目的 研究c9t11-共轭亚油酸（CLA）对人胃腺癌细胞（SGC-7901）侵袭能力的影响，探讨其抑制肿瘤转移的可能机制。方法 用重组基底膜侵袭实验评价癌细胞侵袭能力；用逆转录聚合酶链反应（RT-PCR）检测SGC-7901 细胞中组织基质金属蛋白酶抑制剂（TIMP）-1、TIMP-2 和nm23-H1mRNA 的表达。结果 在200、100和50μmol/L浓度时，c9t11-CLA 对SGC-7901细胞侵袭重组基底膜的抑制率分别为53.7%、40.9%和29.3%。c9，t11-CLA可诱导SGC-7901细胞中TIMP-1、TIMP-2和nm23-H1 mRNA 的表达。结论 c9t11-CLA 抑制SGC-7901细胞侵袭重组基底膜。c9t11-CLA 的抗侵袭活性与诱导肿瘤细胞中TIMP-1、TIMP-2 和nm23-H1 mRNA的表达等有关。

采用体外培养技术，模拟体内肿瘤转移过程，研究共轭亚油酸（conjugated linoliec acid, CLA）对鼠黑色素瘤Bl6-MB高转移细胞系的转移特性，从而探讨CLA预防肿瘤转移的可能途径。研究结果表明，剂量为lOOUmol/L、200Umol/L的CLA可抑制肿瘤细胞增殖、恢复肿瘤细胞间通讯功能、抑制肿瘤细胞向细胞外基质成分[层粘连蛋白（fibronectin, FN）和纤维粘连蛋白（laminin，I.N）]的黏附。

AIM:To explore the inhibition of conjugated linoleic acidisomers in different purity (75% purity c9, t11-, 98% purityc9,t11- and 98% purity t10, c12-CLA) on the formation offorestomach neoplasm and cheopreventive mechanisms. METHODS: Forestomach neoplasm model induced by B(a)P in KunMing mice was established. The numbers of tumorand diameter of each tumor in forestomach were counted;the mice plasma malondialdehyde (MDA) were measuredby TBARS assay; TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1, ERK-1, MKP-1 protein in forestomach neoplasm werestudied by Western Blotting assay.RESULTS: The incidence of neoplasm in B(a)Pgroup, 75%purity c9, t11-CLA group, 98% purity c9,t11-CLA groupand 98% purity t10, c12-CLA group was 100%, 75.0 %(P>0.05), 69.2%(P<0.05) and 53.8%(P<0.05) respectivelyand the effect of two CLA isomers in 98% purity onforestomach neoplasia was significant; CLA showed noinfluence on the average tumor numbers in tumor-bearingmouse, but significantly decreased the tumor size, the tumor average diameter of mice in 75% purity c9,t11-CLA group,98% purity c9,t11-CLA group and 98% purity t10, c12-CLAgroup was 0.157