Swanson Kelly M, Hohl Raymond J
Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA.
Curr Cancer Drug Targets. 2006 Feb;6(1):15-37. doi: 10.2174/156800906775471743.
The mevalonate pathway has become an important target for anti-cancer therapy. Manipulation of this pathway results in alteration of malignant cell growth and survival in cell culture and animal models, with promising potential for application in human cancers. Mevalonate is synthesized from 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA). Mevalonate is further metabolized to farnesyl pyrophosphate (FPP), which is the precursor for sterols. In addition, the farnesyl moiety from FPP is utilized for post-translational modification of proteins including small GTPases, such as Ras and Ras related proteins, which play a role in malignant transformation of cells. FPP is a precursor for geranylgeranyl pyrophosphate (GGPP), which is similarly involved in post-translational modification of proteins. There has been intense interest in manipulating the pathway through HMG-CoA reductase inhibition. More recently, the focus has been on manipulating the pathway by post-translational modification of key regulatory proteins through farnesyl prenyl transferase (FPTase) or geranylgeranyl prenyl transferase (GGPTase) inhibition. This review focuses on the mevalonate pathway and the application of rational drug therapies to manipulate this pathway. Included in the review are a summary of agents demonstrating success in preclinical investigations such as; farnesyl transferase inhibitors, geranylgeranyl transferase inhibitors, dual inhibitors, statins, bisphosphonates, histone deacetylase inhibitors and other compounds. While these agents have shown preclinical success, translation to success in clinical trials has been more difficult. These clinical trials are reviewed along with evaluation of some of the potential problems with these agents in their clinical application.
甲羟戊酸途径已成为抗癌治疗的一个重要靶点。在细胞培养和动物模型中,对该途径的操控会导致恶性细胞生长和存活的改变,在人类癌症应用方面具有广阔的潜力。甲羟戊酸由3-羟基-3-甲基戊二酰辅酶A(HMG-CoA)合成。甲羟戊酸进一步代谢为法尼基焦磷酸(FPP),它是甾醇的前体。此外,FPP中的法尼基部分用于蛋白质的翻译后修饰,包括小GTP酶,如Ras和Ras相关蛋白,它们在细胞的恶性转化中起作用。FPP是香叶基香叶基焦磷酸(GGPP)的前体,GGPP同样参与蛋白质的翻译后修饰。通过抑制HMG-CoA还原酶来操控该途径一直备受关注。最近,重点已转向通过抑制法尼基异戊二烯转移酶(FPTase)或香叶基香叶基异戊二烯转移酶(GGPTase)对关键调节蛋白进行翻译后修饰来操控该途径。本综述聚焦于甲羟戊酸途径以及合理药物疗法在操控该途径方面的应用。综述内容包括在临床前研究中取得成功的药物总结,如法尼基转移酶抑制剂、香叶基香叶基转移酶抑制剂、双重抑制剂、他汀类药物、双膦酸盐、组蛋白去乙酰化酶抑制剂和其他化合物。虽然这些药物在临床前研究中已取得成功,但在临床试验中取得成功却更加困难。本文对这些临床试验进行了综述,并评估了这些药物在临床应用中一些潜在的问题。