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。

AIM:To investigate the effect of c9,t11-conjugatedlinoleic acid (c9,t11-CLA) on the invasion of human gastriccarcinoma cell line and its possible mechanism of preventing metastasis. METHODS: Using reconstituted basement membrane invasion, chemotaxis, adhesion, PAGE substrate zymography and RT-PCR assays, we analyzed the abilities of invasion, direct migration, adhesion of intracellular matrix, as well as the activity of type IV collagenase and expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 mRNA in SGC-7901 cells which were treated with gradually increased concentrations (25, 50, 100 and 200 mmol/L) of c9, t11-CLA for 24h. RESULTS: At the concentrations of 200mmol/L, 100mmol/L and 50 mmol/L, c9,t11-CLA suppressed the invasion of SGC-7901 cells into the reconstituted basement membrane by53.7%, 40.9% and 29.3%, respectively, in comparison with the negative control. Only in the 200 mmol/L c9,t11-CLA group, the chemotaxis of SGC-7901 cells was inhibitedby 16.0% in comparision with the negative control. C9, t11-CLA also could inhibit the adhesion of SGC-7901 cells tolaminin, fibronectin and Matrigel, increase the expressionof TIMP-1 and TIMP-2 mRNA, and reduce type IV collagenaseactivities in the serum-free medium supernatant of SGC-7901 cells.CONCLUSION: c9, t11-CLA can inhibit the invasion of SGC-7901 cells at multiple procedures in tumor metastasiscascade, which may be associated with the induction ofTIMP-1 and TIMP-2 mRNA expression.Chen BQ, Yang YM, Gao YH, Liu JR, Xue YB, Wang XL, ZhengYM, Zhang JS, Liu RH. Inhibitory effects of c9,t11-conjugatedlinoleic acid on invasion of human gastric carcinoma cell lineSGC-7901. World J Gastroenterol 2003;9(9):1909-1914http://www.wjgnet.com/1007-9327/9/1909.asp

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).

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。