Effect of cis-9,trans-11-conjugated linoleic acid on cell cycle of gastric adenocarcinoma cell line(SGC-7901)

AIM: To determine the effect of cis-9, trans-1l-conjugated linoleic acid ( c9, tl 1-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, B1, D1, pl6nink4a and p21clp/wafl ofSGC-7901 cells which were heated with various c9, tll-CLAconcentrations (25,50,100 and 200μnol@L-1)of c9, tll-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, tll-CLA. SGC-7901 cells. Eightday after treatment with various concentrations of c9, tl1-CLA mentioned above, the inhibition rates were 5.92 % ,20.15 % ,75.61% and 82.44 % ,respectively and inhibitory effeotof c9, tll-CLA on DNA synthesis (except for 25 tmol/L,24h) showed significantly less 3H-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,tl1-CLA concentrations at various times significantlydecreased the expressions of PCNA (the expression rateswere7.2-3.0 %,24 h and 9.1-0.9 % at 48 h, respectively),Cyclin A (l1.0-2.3 %, 24 h and 8.5-0.5 % ,48 h), B1 (4.8-1.8% at 24 h and 5.5-0.6 % at 48 h)and D1 (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, B1 and D1were 6.5 % at 24h and 9.0 % at 48 h, 4.2% at 24h and5.1% at 48 h, 9.5 % at 24h and 6.0 % at 48 h,respectively)(P＜ 0.01), whereas the expressions of p16ink4a and p21clp/waf1,cyclin-dependent kinases inhibltors(CDKI), were increased.CONCLUSION: The cell growth and proliferation of SGC-7901cell is inhibited by c9, tll-CLA via blocking the cell cycle,with reduced expressions of cyclin A, B1 and D1 andenhanced expressions of CDKI( p16ink4a and p21cip/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 immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B(1), D(1), p16(ink4a) and p21(cip/waf1) of SGC-7901 cells which were treated with various c9, t11-CLA concentrations (25, 50, 100 and 200 micromol.L(-1))of c 9, t 11-CLA for 24 and 48h, 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. Eight day 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 and inhibitory effect of c9, t11-CLA on DNA synthesis (except for 25 micromol.L, 24h) showed significantly less (3)H-TdR incorporation than that in the negative controls (P<0.05 and P<0.01). Immunocytochemical staining demonstrated that SGC-7901 cells preincubated in media supplemented with different c9, t11-CLA concentrations at various times significantly decreased the expressions of PCNA (the expression rates were 7.2-3.0%, 24h and 9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24h and 8.5-0.5%,48h), B(1) (4.8-1.8% at 24h and 5.5-0.6% at 48h)and D(1) (3.6-1.4% at 24h and 3.7%-0 at 48h) as compared with those in the negative controls(the expressions of PCNA, Cyclin A, B(1) and D(1) were 6.5% at 24h 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 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 c9, t11-CLA via blocking the cell cycle, with reduced expressions of cyclin A,B(1) and D(1) and enhanced expressions of CDKI(P16(ink4a) and p21(cip/waf1)).