AIM: To determine the effect of cis-9,trans-11-conjugated linoleic acid (c9, t11-CLA) on the cell cycleof gastric cancer cells(SGC-7901)and its possiblemechanism in inhibition cancer growth. METHODS: Using cell culture andimmunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, P16ink4aand p21cip/waf1 of SGC-7901 cells which were treatedwith various c9,t11-CLA concentrations (25, 50, 100 and 200μmol·L-1) of c9, t11-CLA for 24 and 48h, with anegative control (0.1% ethane). RESULTS: The cell growth and DNA synthesis of SGC-7901cells were inhibited by c9, t11-CLA. SGC-7901 cells. Eightday after treatment with various concentrations of c9, t11-CLA mentioned above, the inhibition rates were 5.92%, 20.15%, 75.61% and 82.44%,respectively andinhibitory effect of c9, t11-CLA on DNA synthesis (exceptfor 25μmol/L,24h) showed significantly less 3H-TdRincorporation than that in the negative controls (P<0.05 and P<0.01). Immunocytochemical stainingdemonstrated that SGC-7901 cells preincubated in mediasupplemented with different c9,t11-CLA concentrationsat varioustimes significantly decreased the expressionsof PCNA (the expression rates were 7.2-3.0%,24h and9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24hand 8.5-0.5%, 48h), B1 (4.8-1.8% at 24h and 5.5-0.6%at 48h) and D1 (3.6-1.4% at 24h and 3.7%-0 at 48h) ascompared with those in the negative controls(theexpressions of PCNA, Cyclin A, B1 and D1 were 6.5% at24h and 9.0% at 48h, 4.2% at 24h and 5.1% at 48h,9.5% at 24h and 6.0% at 48h, respectively) (P<0.01), whereas the expressions of p16ink4a and p21cip/waf1, cyclindependentkinases inhibitors(CDKI), were increased. CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c9,t11-CLA via blocking the cellcycle, with reduced expressions of cyclin A,B1 and D1 andenhanced expressions of CDKI(p16ink4a and p21cip/waf1).

AIM: To determine the effect of apoptosis on gastric cancercells (SGC-7901) induced by cis-9, trans-11-conjugatedlinoleic acid (c9, t11-CLA) and its possible mechanism in theinhibition of cancer cells growth. METHODS: Using cell culture, flow cytometery andimmunocytochemical techniques, we examined the cellgrowth, frequency of apoptosis and distribution of cell cycle,expression of ki67, bcl-2, Fas, and c-myc of SGC-7901 cellswhich were treated with various c9, t11-CLA concentrations(25,50,100 and 200 mmol

Objectives:To determine the effect of cis-9, trans-11-conjugated linoleic acid on the cell cycle ofmammary cancer cells (MCF-7) and its possible mechanism of inhibition cancer growth. Methods:Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, p16ink4aand p21cip/waf1of MCF-7 cells which were treatedwith various c9, t11-CLA concentrations (25mM, 50mM, 100mM and 200 M) of c9, t11-CLA for 24 and48 h, with negative controls (0.1% ethanol). Results: The cell growth and DNA ynthesis of MCF-7 cells were inhibited by c9, t11-CLA. MCF-7cells, after treatment with various c9, t11-CLA doses mentioned above for 8 days, the nhibition frequencywas 27.18%, 35.43%, 91.05%, and 92.86%, respectively and the inhibitory effect of c9,t11-CLA on DNA synthesis (except for 25mM, 24 h) incorporated significantly less3H-TdR than did the negative control(P<0.05 and P<0.01). To furtherinvestigate the influence on the cell cycle progression, we found that c9, t11-CLA may arrest the cell cycle of MCF-7 cells. Immunocytochemical staining demonstrated that MCF-7 cellspreincubated in media supplemented with different c9, t11-CLA concentrations at various times significantlydecreased the expressions of PCNA, and Cyclin A, B1, D1compared with the negative controls(P<0.01), whereas the expressions of p16ink4aand p21cip/waf1, cyclin-dependent kinases inhibitors (CDKI),were increased. Conclusions: The cell growth and proliferation of MCF-7 cellsis inhibited by c9, t11-CLA by blockingthe cell cycle, which reduces expressions of cyclin A, B1, D1and enhances expressions of CDKI (p16ink4aandp21cip/waf1).

目的 用苯并（a）芘〔B（a）P〕建立小鼠前胃癌模型，观察不同构成的共轭亚油酸（CLA）对前胃癌的抑制作用以及与脂质过氧化的关系。方法 通过灌胃方式给予昆明种小鼠B(a)p，建立前胃癌模型。用光学显微镜作病理组织检查，用比色法测定丙二醛（MDA）含量。结果 利用B(a)p 成功地在昆明种小鼠体内建立了前胃癌模型，病理结果分析表明所建立的前胃癌为鳞状细胞癌；小鼠前胃肿瘤的计数结果表明，B(a)p 组，75% c9，tll-CLA组，98% t10，c12-ClA组的肿瘤发生率分别为!100%，75.0%，69.2%和53.8%并且75%c9，t11-CLA，98%c9，98%t10，c12-CLA明显降低前胃肿瘤的直径，但对荷瘤小鼠的平均荷瘤数没有影响；与阴性对照组和B（a）P对照组相比，CLA处理能提高小鼠体内MDA含量。结论 B（a）P诱导昆明种小鼠的前胃组织形成鳞状细胞癌；不同构成CLA对B（a）P诱导小鼠前胃癌均具有抑制作用，并且MDA可能是CLA发挥预防肿瘤作用的可能机理之一。

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。