AIM:To determine the effect of cis-9,trans-11-conjugatedlinoleic acid(c9,t11-CLA)on the cell cycle of gastric cancercells(SGC-7901)and its possible mechanism in inhibitioncancer growth.METHODS:Using cell culture and immunocytochemicaltechniques,we examined the cell growth,DNA synthesis,expression of PCNA,cyclin A,B_1,D_1,p16~(ink4a)and p21~(cip/waf1)ofSGC-7901 cells which were treated with various c9,t11-CLAconcentrations(25,50,100 and 200μmol·L~(-1))of c9,t11-CLA for 24and 48 h,with a negative 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,t1’-CLA mentioned above,the inhibition rates were 5.92 %,2■15 %,75.51 % and 82.44 %,respectively and inhibitory effe■tof c9,t11-CLA on DNA synthesis(except for 25 μmol/L,24h)showed significantly less ~3 H-TdR incorporation than thatin the negative controls(P<0.05 and P<0.01).Immunocytochemical staining demonstrated that SGC-7901cells preincubated in media supplemented with different c9,t11-CLA concentrations at various times significantlydecreased the expressions of PCNA(the expression rateswere 7.2-3.0 %,24 h and 9.1-0.9 % at48 h,respectively),Cyclin A(11.0-2.3 %,24 h and 8.5-0.5 %,48 h),B_1(4.8-1.8% at 24 h and 5.5-0.6 % at 48 h)and D_1(3.6-1.4 % at 24 hand 3.7 %-0 at 48 h)as compared with those in the negativecontrols(the expressions of PCNA,Cyclin A,B_1 and D_1were 6.5 % at 24h and 9.0 % at 48 h,4.2% at 24h and 5.1% at 48 h,9.5 % at 24 h and 6.0 % at 48 h,respectively)(P<0.01),whereas the expressions of p16~(ink4a)and p21~(cip/waf1),cyclin-dependent kinases inhibitors(CDKI),were increased.CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c_9, fll-CLA via blocking the cell cycle, with reduced expressions of cyclin A, B_1, and D_1, and enhanced expressions of CDKI( p16~(inkta) and P21~(cip/waf1)). AIM: To determine the effect of cis-9, trans-11-conjugated linoleic acid (c9, t11-CLA) on the cell cycle of gastric cancer cells (SGC-7901) and its possible mechanism in inhibition cancer growth. METHODS: Using cell culture and immunocytochemicaltechniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B_1, D_1, p16 ~ (ink4a) and p21 ~ (cip / waf1) ofSGC-7901 cells which were treated with various c9, t11-CLAconcentrations 25, 50, 100 and 200 μmol·L -1 of c9, t11-CLA for 24 and 48 h, with a negative control (0 1% ethane) RESULTS: The cell growth and DNA synthesis of SGC-7901 cells were inhibited by c9 , t11-CLA. SGC-7901 cells. Eightday after treatment with various concentrations of c9, t1’-CLA mentioned above, the inhibition rates were 5.92%, 2 ■ 15%, 75.51% and 82.44% c9, t11-CLA on DNA synthesis (except for 25 μmol / L, 24h) showed significantly less ~ 3 H-TdR incorporation than that of the negative controls (P <0.05 and P <0.01) rated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations at various times significantly established the expressions of PCNA (the expression rateswere 7.2-3.0%, 24 h and 9.1-0.9% at 48 h, respectively), Cyclin A ( 11.0-2.3%, 24 h and 8.5-0.5%, 48 h), B_1 (4.8-1.8% at 24 h and 5.5-0.6% at 48 h) and D_1 (3.6-1.4% at 24 hand 3.7% -0 at 48 h) as compared with those in the negative controls (the expressions of PCNA, Cyclin A, B_1 and D_1were 6.5% at 24h and 9.0% at 48 h, 4.2% at 24h and 5.1% at 48 h, 9.5% at 24 h and 6.0% at 48 h, respectively) (P <0.01), while the expressions of p16 ~ (ink4a) and p21 ~ (cip / waf1), cyclin-dependent kinases inhibitors proliferation of SGC-7901 cells is inhibited by c_9, fll-CLA via blocking the cell cycle with reduced expressions of cyclin A, B_1, and D_1, and enhanced expressions of CDKI (p16 ~ inkta) and P21 ~ (cip / waf1 )).