Li Zhiming, Lin Qing, Ma Qilin, Lu Congxia, Tzeng Chi-Meng
School of Pharmaceutical Sciences, Xiamen University, Xiamen 361005, Fujian, China.
Curr Cancer Drug Targets. 2014;14(3):310-21. doi: 10.2174/1568009614666140312145936.
Parkinson's disease (PD) and cancer are often thought of as two sides of the same coin. At first glance, cancer and PD appear to have little in common. PD is caused by the degeneration of dopaminergic neurons, whereas cancer results from the uninhibited growth of tumor cells. Increasing numbers of genetic studies suggest that the pathogenesis of PD and cancer may involve similar genes, pathways, and mechanisms. The differences in the pathological and cellular mechanisms, and the associated genetic mutations, may result in two such divergent diseases. In this article, we highlight some molecular mechanisms and key biomarkers which might cause those two diseases from misfolding and degradation of proteins, mitochondrial damage, oxidative stress response, cell cycle control and DNA repair, and the PI3K/AKT/ mTOR pathway, in order to provide help to the understanding and treatment of these two diseases.
帕金森病(PD)和癌症常被视为同一枚硬币的两面。乍一看,癌症和帕金森病似乎没有什么共同之处。帕金森病是由多巴胺能神经元变性引起的,而癌症则是肿瘤细胞不受抑制生长的结果。越来越多的遗传学研究表明,帕金森病和癌症的发病机制可能涉及相似的基因、途径和机制。病理和细胞机制以及相关基因突变的差异,可能导致这两种截然不同的疾病。在本文中,我们重点介绍了一些分子机制和关键生物标志物,它们可能从蛋白质的错误折叠和降解、线粒体损伤、氧化应激反应、细胞周期控制和DNA修复以及PI3K/AKT/mTOR途径等方面引发这两种疾病,以便为这两种疾病的理解和治疗提供帮助。