咖喱是多种香料的混合物。它之所以具有杀死癌细胞的作用，主要归功于其配料中黄姜所含的姜黄素。大多数情况下，令癌细胞死亡的方法是通过激活细胞中的半胱氨酸蛋白酶（又称凋亡蛋白酶），从而启动癌细胞自身程序性凋亡。
爱尔兰科克癌症研究中心研究员杰拉尔丁·奥沙利文科因和他的研究小组在试验中发现，经过姜黄素处理的癌细胞在24小时内开始死亡，而其中半胱氨酸蛋白酶水平并没有提高。不仅如此，研究人员即使使用其他药物阻止半胱氨酸蛋白酶启动程序性凋亡，癌细胞还是会死亡。这说明姜黄素可以通过另一种全新途径杀死癌细胞。
科学家并非近期才意识到姜黄素具有医学价值。这项研究的另一名负责人莎伦·麦克纳说：“医学界早已意识到某些天然物质对治疗癌症具有潜在价值，并且认为姜黄素可能就是其中一种。”先前曾有研究称姜黄素对癌细胞有抑制作用，并指出常吃咖喱的人不易患癌症。可惜当咖喱被人体消化吸收后，这种抗癌特性也就很快消失。2007年美国科学家发现，姜黄素有助老年痴呆症患者提高免疫力。还有人尝试用姜黄素治疗关节炎。麦克纳说，姜黄素利用一种未知的“细胞语言”向癌细胞发出“死亡信号”。他们的研究表明可以直接从咖喱中提取姜黄素来研发治疗癌症的新药。（生物谷Bioon.com）
相关信息：
细胞凋亡分子机制
细胞凋亡与肿瘤
细胞凋亡研究：
Cell：细胞坏死状凋亡分子机制
Nature Cell Biology：动植物的细胞凋亡方式相同
Science：RIP3具有细胞凋亡/细胞坏死开关作用
更多：细胞凋亡专题
细胞凋亡试剂大全
细胞凋亡检测技术与方法
姜黄与癌症：
咖喱粉中姜黄色素可抑制癌细胞生长
JBC：咖喱--对抗早老性痴呆的新武器
Janus激酶细胞信号转导及转录活化因子通路抑制剂的研究进展
生物谷推荐原始出处：
British Journal of Cancer (2009) 101, 1585–1595. doi:10.1038/sj.bjc.6605308
Curcumin induces apoptosis-independent death in oesophageal cancer cells
G O'Sullivan-Coyne1, G C O'Sullivan1, T R O'Donovan1, K Piwocka2 and S L McKenna1
1Leslie C. Quick Laboratory, Cork Cancer Research Centre, BioSciences Institute, University College Cork and Mercy University Hospital, Cork, Ireland
2Nencki Institute of Experimental Biology, Warsaw, Poland
background: Oesophageal cancer incidence is increasing and survival rates remain extremely poor. Natural agents with potential for chemoprevention include the phytochemical curcumin (diferuloylmethane). We have examined the effects of curcumin on a panel of oesophageal cancer cell lines.
methods: MTT (3-(4,5-dimethyldiazol-2-yl)-2,5 diphenyl tetrazolium bromide) assays and propidium iodide staining were used to assess viability and DNA content, respectively. Mitotic catastrophe (MC), apoptosis and autophagy were defined by both morphological criteria and markers such as MPM-2, caspase 3 cleavage and monodansylcadaverine (MDC) staining. Cyclin B and poly-ubiquitinated proteins were assessed by western blotting.
results: Curcumin treatment reduces viability of all cell lines within 24 h of treatment in a 5–50 m range. Cytotoxicity is associated with accumulation in G2/M cell-cycle phases and distinct chromatin morphology, consistent with MC. Caspase-3 activation was detected in two out of four cell lines, but was a minor event. The addition of a caspase inhibitor zVAD had a marginal or no effect on cell viability, indicating predominance of a non-apoptotic form of cell death. In two cell lines, features of both MC and autophagy were apparent. Curcumin-responsive cells were found to accumulate poly-ubiquitinated proteins and cyclin B, consistent with a disturbance of the ubiquitin–proteasome system. This effect on a key cell-cycle checkpoint regulator may be responsible for the mitotic disturbances and consequent cytotoxicity of this drug.
conclusion: Curcumin can induce cell death by a mechanism that is not reliant on apoptosis induction, and thus represents a promising anticancer agent for prevention and treatment of oesophageal cancer.
