Moragoda L, Jaszewski R, Majumdar A P
Department of Medicine, Wayne State University School of Medicine, Detroit, Michigan, USA.
Anticancer Res. 2001 Mar-Apr;21(2A):873-8.
We have investigated the chemopreventive role of curcumin in gastrointestinal cancers by studying the regulation of proliferation and apoptosis in gastric (KATO-III) and colon (HCT-116) cancer cells. Curcumin inhibited cell proliferation and induced G2/M arrest in HCT-116 cells. Investigation of the levels of cyclins E, D and B by immunoblot analysis showed cyclin B level was unaffected, whereas cyclin D and E levels declined with curcumin in both cell lines. Investigation of cyclin-dependent kinases, Cdk2 and Cdc2, showed activity of Cdc2, but not Cdk2, increased markedly in response to curcumin. In both cell lines, immunoblot analysis indicated that curcumin caused induction of apoptosis as evidenced by cleavage of PARP, caspase-3, and reduction in Bcl-XL levels. Curcumin also stimulated the activity of caspase-8, which initiates Fas signalling pathway of apoptosis. Curcumin therefore appears to exert its anticarcinogenic properties by inhibiting proliferation and inducing apoptosis in certain gastric and colon cancer cells.
我们通过研究姜黄素对胃癌（KATO-III）和结肠癌（HCT-116）细胞增殖和凋亡的调控作用，来探究其在胃肠道癌症中的化学预防作用。姜黄素抑制HCT-116细胞的增殖并诱导其G2/M期阻滞。通过免疫印迹分析检测细胞周期蛋白E、D和B的水平，结果显示细胞周期蛋白B的水平未受影响，而在两种细胞系中，细胞周期蛋白D和E的水平随姜黄素处理而下降。对细胞周期蛋白依赖性激酶Cdk2和Cdc2的研究表明，Cdc2的活性而非Cdk2的活性在姜黄素处理后显著增加。在两种细胞系中，免疫印迹分析表明姜黄素可诱导凋亡，这可通过PARP、caspase-3的裂解以及Bcl-XL水平的降低得以证明。姜黄素还刺激了caspase-8的活性，该酶启动凋亡的Fas信号通路。因此，姜黄素似乎通过抑制某些胃癌和结肠癌细胞的增殖并诱导其凋亡来发挥抗癌特性。
