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).