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).