Induction and transmission of oncogene-induced senescence

被引:16
作者
Rattanavirotkul, Nattaphong [1 ]
Kirschner, Kristina [2 ]
Chandra, Tamir [3 ]
机构
[1] Mahidol Univ, Ramathibodi Hosp, Ramathibodi Med Sch, Chakri Naruebodindra Med Inst,Fac Med, 111 Bang Pla, Bang Phli 10540, Samut Prakan, Thailand
[2] Univ Glasgow, Inst Canc Sci, Glasgow G61 1BD, Lanark, Scotland
[3] Univ Edinburgh, MRC Inst Genet & Mol Med, MRC Human Genet Unit, Edinburgh, Midlothian, Scotland
基金
英国惠康基金;
关键词
Oncogene-induced senescence; Secondary senescence; Notch signalling; Juxtacrine senescence; CELLULAR SENESCENCE; SECRETORY PHENOTYPE; TUMOR-SUPPRESSOR; OXIDATIVE STRESS; HUMAN-CELLS; BIOMARKER; P53; RESTORATION; CLEARANCE; MUTATIONS;
D O I
10.1007/s00018-020-03638-0
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
Senescence is a cellular stress response triggered by diverse stressors, including oncogene activation, where it serves as a bona-fide tumour suppressor mechanism. Senescence can be transmitted to neighbouring cells, known as paracrine secondary senescence. Secondary senescence was initially described as a paracrine mechanism, but recent evidence suggests a more complex scenario involving juxtacrine communication between cells. In addition, single-cell studies described differences between primary and secondary senescent end-points, which have thus far not been considered functionally distinct. Here we discuss emerging concepts in senescence transmission and heterogeneity in primary and secondary senescence on a cellular and organ level.
引用
收藏
页码:843 / 852
页数:10
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