Public Health College of Harbin Medical University, 199 Dongdazhi Street, Nangang District, Harbin, Heilongijang, P.R. China,
Environ Health Prev Med. 2002 Nov;7(5):205-10. doi: 10.1007/BF02898006.
To determine the effect of cis-9, trans-11-conjugated linoleic acid on the cell cycle of mammary cancer cells (MCF-7) and its possible mechanism of 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/wafl) of MCF-7 cells which were treated with various c9, t11-CLA concentrations (25 mM, 50 mM, 100 mM and 200 mM) of c9, t11-CLA for 24 and 48 h, with negative controls (0.1% ethanol).
The cell growth and DNA synthesis of MCF-7 cells were inhibited by c9, t11-CLA. MCF-7 cells, after treatment with various c9, t11-CLA doses mentioned above for 8 days, the inhibition frequency was 27.18%, 35.43%, 91.05%, and 92.86%, respectively and the inhibitory effect of c9, t11-CLA on DNA synthesis (except for 25 mM, 24 h) incorporated significantly less(3)H-TdR than did the negative control (P<0.05 andP<0.01). To further investigate 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 cells preincubated in media supplemented with different c9, t11-CLA concentrations at various times significantly decreased the expressions of PCNA, and Cyclin, A, B(1), D(1) compared with the negative controls (P<0.01), whereas the expressions of p16(ink4a) and p21(cip/wafl), cyclin-dependent kinases inhibitors (CDKI), were increased.
The cell growth and proliferation of MCF-7 cells is inhibited by c9, t11-CLA by blocking the cell cycle, which reduces expressions of cyclin A, B(1), D(1) and enhances expressions of CDKI (p16(ink4a) and p21(cip/wafl)).
研究顺-9，反-11 共轭亚油酸（c9，t11-CLA）对乳腺癌细胞（MCF-7）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，观察不同浓度（25、50、100、200mM）c9，t11-CLA 作用于 MCF-7 细胞 24 和 48 小时后细胞生长、DNA 合成、PCNA、细胞周期蛋白 A、B（1）、D（1）、p16（ink4a）和 p21（cip/wafl）的表达情况，并设阴性对照（0.1%乙醇）。
c9，t11-CLA 抑制 MCF-7 细胞的生长和 DNA 合成。经上述不同剂量 c9，t11-CLA 处理 MCF-7 细胞 8 天后，抑制率分别为 27.18%、35.43%、91.05%和 92.86%，c9，t11-CLA 对 DNA 合成的抑制作用（除 25mM，24 小时外）明显低于阴性对照组（P<0.05 和 P<0.01）。为进一步探讨对细胞周期进程的影响，我们发现 c9，t11-CLA 可能使 MCF-7 细胞周期阻滞。免疫细胞化学染色显示，与阴性对照组相比，预先用不同浓度 c9，t11-CLA 孵育培养基的 MCF-7 细胞 PCNA 和细胞周期蛋白 A、B（1）、D（1）的表达明显降低（P<0.01），而细胞周期蛋白依赖性激酶抑制剂（CDKI）p16（ink4a）和 p21（cip/wafl）的表达增加。
c9，t11-CLA 通过阻断细胞周期抑制 MCF-7 细胞的生长和增殖，降低细胞周期蛋白 A、B（1）、D（1）的表达，增强 CDKI（p16（ink4a）和 p21（cip/wafl））的表达。
