静止期癌细胞(QCC)的残留和重新增殖是导致癌症复发的重要原因，目前尚无针对QCC的药物。前期工作中，我们报道了云南藤黄中的Guttiferone K(GUTK)具有抑制QCC激活从而抑制前列腺癌的作用；后续研究发现GUTK不仅可在体外选择性杀死化疗药物耐受的QCC，动物实验中也能抑制化疗后的肿瘤复发。蛋白组学发现GUTK主要作用于线粒体核糖体通路，下调了10个线粒体核糖体家族蛋白(MRPs)。为阐明GUTK如何调控MRPs及MRPs在QCC存活中的作用，本研究将采用BIAcore SPR技术，研究GUTK与MRPs蛋白的亲和能力；结合BN-PAGE，免疫印迹，35S氨基酸标记，构建Dox-诱导的基因表达系统等技术，探讨体内外GUTK诱导QCC死亡的作用机理。本项目的成果将为GUTK开发成抑制癌症复发的药物提供理论依据。MRPs作用的阐明将为预防癌症复发药物的筛选提供新靶标和新思维。

The survival and re-proliferation of Quiescent Cancer Cell (QCC) has been concerned as a main cause of cancer recurrence. Unfortunately, there is no effective drug specifically target on QCC. In our previously study, we have identified that Guttiferone K(GUTK), isolated from Garcinia yunnanensis Hu, could inhibit prostate cancer by blocking reactivation of QCC. We also found GUTK could specifically induce chemo-resistant QCC death in vitro and prevent cancer recurrence after chemotherapy in vivo. Proteomics results show that GUTK may target on mitochondrial ribosomal pathway. As many as ten mitochondrial ribosomal protein (MRPs) were down regulated after GUTK treatment. Based on the research work above, this project will further investigate the mechanism of GUTK on MRPs by using multiple techniques, including BIAcore SPR, BN-PAGE, Western blot, 35S-labelled amino acid and Dox-inducible gene expression system. The underlying molecular mechanisms of the inhibitory effect of GUTK on cancer recurrence will be explored in animal model. The achievements of the project could provide the scientific basis for indicating that GUTK acts as a promising agent on preventing cancer recurrence, and suggest MRPs as new target for the drug screening on cancer recurrence prevention, which could in turn enlighten a new mode of cancer therapy.