Molecular crosstalk between cancer and neurodegenerative diseases

被引:68
|
作者
Seo, Jiyeon [1 ,3 ]
Park, Mikyoung [1 ,2 ]
机构
[1] Korea Inst Sci & Technol, Brain Sci Inst, Ctr Funct Connect, Seoul 02792, South Korea
[2] Korea Univ Sci & Technol, Dept Neurosci, Daejeon 34113, South Korea
[3] Korea Inst Sci & Technol, Brain Sci Inst, Ctr Neurosci, Seoul 02792, South Korea
基金
新加坡国家研究基金会;
关键词
Age-related diseases; Cell death; Cell survival; Redox system; Glioma; Neurotoxicity; PROLYL-ISOMERASE PIN1; PROTEIN PHOSPHATASE 2A; WEIGHT CYCLIN-E; AMYLOID-PRECURSOR-PROTEIN; F-MEDIATED DEGRADATION; A-ALPHA SUBUNIT; MUTANT P53; CELL-CYCLE; BREAST-CANCER; ALZHEIMER-DISEASE;
D O I
10.1007/s00018-019-03428-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The progression of cancers and neurodegenerative disorders is largely defined by a set of molecular determinants that are either complementarily deregulated, or share remarkably overlapping functional pathways. A large number of such molecules have been demonstrated to be involved in the progression of both diseases. In this review, we particularly discuss our current knowledge on p53, cyclin D, cyclin E, cyclin F, Pin1 and protein phosphatase 2A, and their implications in the shared or distinct pathways that lead to cancers or neurodegenerative diseases. In addition, we focus on the inter-dependent regulation of brain cancers and neurodegeneration, mediated by intercellular communication between tumor and neuronal cells in the brain through the extracellular microenvironment. Finally, we shed light on the therapeutic perspectives for the treatment of both cancer and neurodegenerative disorders.
引用
收藏
页码:2659 / 2680
页数:22
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