JS-K抗肿瘤效果机制的研究进展

研究显示一氧化氮(NO)在体内参与多种信号通路的传导,在机体的肿瘤形成等多种病理和生理过程中发挥着重要作用。谷胱甘肽-S-转移酶(GSTs)在很多肿瘤的表达都是升高的,在肿瘤细胞中发挥着维持氧化还原平衡、解毒和促使肿瘤细胞发生耐药等方面的的作用;而JS-K是近年来新合成的一种一氧化氮(NO)前体药,其可以在体内被谷胱甘肽-S-转移酶(GSTs)酶解生成NO,进而发挥抗肿瘤效应。研究显示JS-K对机体的多种肿瘤都表现出明显的抑制作用,而对正常的组织则没有明显的损伤作用。由于肿瘤的组织来源不同,JS-K表现出的杀伤肿瘤的机制也不尽相同。本课题组通过广泛的文献阅读,系统地综述JS-K杀伤各系统肿瘤的作用机制,为JS-K杀伤肿瘤的进一步的机制研究提供一些有益的思路,和为将来JS-K的临床应用提供理论基础。

Research Progress of JS-K as Anticancer Agents

ABSTRACT: Previous studies have shown nitric oxide (NO) is involved in a variety of signal pathways in vivo, and plays an impor- tant role in lots of pathological and physiological processes, such as tumorigenesis and so on. The expression of glutathione S-transferase (GSTs) is upregulated in many tumors, which plays an important role in maintaining the balance of redox, detoxification, and resistence to chemotherapeutics for the tumor cells. In recent years, a novel NO prodrug named JS-K was synthesised, and JS-K can be selectively catalysed by GSTs, then NO is released, subsequently showing the anticancer effect. Many studies have demonstrated JS-K can inhibit the growth of a broad spectrum of tumors, while sparing the normal tissue cells. The mechanisms for JS-K to kill tumor cells are not al- ways the same due to the differenrt origins of tumors in different systems. In this study, our team systemically reviewed the mechanisms for JS-K to kill tumors originating from different systems through extensive literature reading, with the purpose to providing some helpful ideas for the further study of JS-K and theoretical foundation for JS-K in the future clinical use.