Liu Jia-Ren, Li Bai-Xiang, Chen Bing-Qing, Han Xiao-Hui, Xue Ying-Ben, Yang Yan-Mei, Zheng Yu-Mei, Liu Rui-Hai
Department of Toxicological Health, Public Health College, Harbin Medical University, 199 Dongdazhi Street, Nangang District, Harbin 150001, Heilongjiang Province, China.
World J Gastroenterol. 2002 Apr;8(2):224-9. doi: 10.3748/wjg.v8.i2.224.
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.
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).
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.
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)).
确定顺-9，反-11-共轭亚油酸（c9，t11-CLA）对胃癌细胞（SGC-7901）细胞周期的影响及其抑制肿瘤生长的可能机制。
采用细胞培养和免疫细胞化学技术，检测用不同浓度（25、50、100和200μmol·L⁻¹）的c9，t11-CLA处理24小时和48小时的SGC-7901细胞的生长、DNA合成、增殖细胞核抗原（PCNA）、细胞周期蛋白A、B1、D1、p16（ink4a）和p21（cip/waf1）的表达，以阴性对照（0.1%乙烷）作为对照。
c9，t11-CLA抑制SGC-7901细胞的生长和DNA合成。用上述不同浓度的c9，t11-CLA处理8天后，抑制率分别为5.92%、20.15%、75.61%和82.44%，且c9，t11-CLA对DNA合成的抑制作用（25μmol·L，24小时除外）显示³H-TdR掺入量明显低于阴性对照（P<0.05和P<0.01）。免疫细胞化学染色表明，在不同时间用添加不同浓度c9，t11-CLA的培养基预孵育的SGC-7901细胞，与阴性对照相比，PCNA（24小时表达率为7.2-3.0%，48小时为9.1-0.9%）、细胞周期蛋白A（24小时为11.0-2.3%，48小时为8.5-0.5%）、B1（24小时为4.8-1.8%，48小时为5.5-0.6%）和D1（24小时为3.6-1.4%，48小时为3.7%-0）的表达显著降低（P<0.01），而细胞周期蛋白依赖性激酶抑制剂（CDKI）P16（ink4a）和P21（cip/waf1）的表达增加。
c9，t11-CLA通过阻断细胞周期抑制SGC-7901细胞的生长和增殖，使细胞周期蛋白A、B1和D1的表达降低，细胞周期蛋白依赖性激酶抑制剂P16（ink4a）和p21（cip/waf1）的表达增加。
