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-mycof SGC-7901 cellswhich were treated with various c9,t11-CLA concentrations(25,50,100 and 200 μmol·L~(-1))of c9,t11-CLA for 24h and 48 h,with a negative control(0.1% ethanol).RESULTS:The growth of SGC-7901 cells was inhibited byc9,t11-CLA.Eight days after treatment with variousconcentrations of c9,t11-CLA,as mentioned above,theinhibition rates were 5.9 %,20.2 %,75.6 % and 82.4 %,respectively.The frequency of apoptosis on SGC-7901 cellsinduced by different concentrations of c9,t11-CLA(exceptfor 25 μmol·L~(-1),24 h)was significantly greater than that inthe negative control(P<0.01).To further investigate theinfluence of the cell cycle progression,we found thatapoptosis induced by c9,t11-CLA may be involved in blockingthe cell cycle of SGC-7901 cells.Immunocytochemical stainingdemonstrated that SGC-7901 cells preincubated in mediasupplemented with different c9,t11-CLA concentrations forvarious time periods significantly decreased the expressionsof ki67(the expression rates were 18.70-3.20 %,at 24 h and8.10-0.20 % at 48 h,respectively),bcl-2(4.30-0.15 % at 24h and 8.05 %-0 at 48 h),and c-myc(4.85-2.20 % at 24 h and4.75-0.30 % at 48 h)as compared with those in the controls(the expressions of ki67,bcl-2,and c-mycwere 15.1% at24 h and 13.5 % at 48 h,6.80 % at 24 h and 8.00 % at 48 h,5.50 % at 24 h and 5.30 % at 48 h,respectively)(P<0.01),whereas the expressions of Fas were increased(0.60-2.75 %,24 h and 0.45-5.95 %,48 h).CONCLUSION:The growth and proliferation of SGC-7901cells are inhibited by c9,t11-CLA via blocking the cell cycle,pathways of bcl-2-associated mitochondria with reduced expression of bcl-2 and Fas-associated death domain protein(FADD)with enhanced expression of Fas.But expression ofc-myc on SGC-7901 cells is lower than that in negativecontrol,which needs to be studied further. AIM: To determine the effect of apoptosis on gastric cancer cells (SGC-7901) induced by cis-9, trans-11-conjugated linoleic acid (c9, t11- CLA) and its possible mechanism in the inhibition of cancer cell growth. METHODS: Using cell culture, flow cytometery and immunocytochemical techniques, we examined the cell growth, frequency of apoptosis and distribution of cell cycle, expression of ki67, bcl-2, Fas, and c- mycof SGC-7901 cellswhich were treated with various c9, 25,50,100 and 200 μmol·L -1 of c9, t11-CLA for 24h and 48 h with a negative control (0.1% ethanol) .RESULTS: The growth of SGC-7901 cells was inhibited byc9, t11 The light of after treatment with various concentrations of c9, t11-CLA, as above, the prohibition rates were 5.9%, 20.2%, 75.6% and 82.4%, respectively. The frequency of apoptosis on different concentrations of SGC-7901 c9, t11-CLA (except for 25 μmol·L -1, 24 h) was significantly greater than that of inthe negative control (P <0.01) .To further inve stigate the effect of the cell cycle progression, we found that apoptosis induced by c9, t11-CLA may be involved in blocking the cell cycle of SGC-7901 cells. Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in mediasupplemented with different c9, t11-CLA concentrations forvarious time periods significantly decreased the expressions of ki67 (the expression rates were 18.70-3.20% at 24 h and 8.10-0.20% at 48 h, respectively), bcl-2 (4.30-0.15% at 24h and 8.05% -0 at 48 and c-myc (4.85-2.20% at 24 h and 4.75-0.30% at 48 h) as compared with those in the controls (the expressions of ki67, bcl-2, and c-mycwere 15.1% at 24 h and 13.5% at 48 h, 6.80% at 24 h and 8.00% at 48 h, 5.50% at 24 h and 5.30% at 48 h, respectively) (P <0.01), while the expressions of Fas were increased (0.60-2.75 %, 24 h and 0.45-5.95%, 48 h) .CONCLUSION: The growth and proliferation of SGC-7901 cells are inhibited by c9, t11-CLA via blocking the cell cycle, pathways of bcl- 2-associated mitochondria with reducer cedexpression of bcl-2 and Fas-associated death domain protein (FADD) with enhanced expression of Fas. But expression of c-myc on SGC-7901 cells is lower than that in negative control, which needs to be studied further.