Tissue‐disruption‐induced cellular stochasticity and epigenetic drift: Common origins of aging and cancer?,BioEssays

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Tissue‐disruption‐induced cellular stochasticity and epigenetic drift: Common origins of aging and cancer?
BioEssays ( IF 3.2 ) Pub Date : 2020-10-29 , DOI: 10.1002/bies.202000140
Jean-Pascal Capp ₁ , Frédéric Thomas ₂

Affiliation

Age‐related and cancer‐related epigenomic modifications have been associated with enhanced cell‐to‐cell gene expression variability that characterizes increased cellular stochasticity. Since gene expression variability appears to be highly reduced by—and epigenetic and phenotypic stability acquired through—direct or long‐range cellular interactions during cell differentiation, we propose a common origin for aging and cancer in the failure to control cellular stochasticity by cell–cell interactions. Tissue‐disruption‐induced cellular stochasticity associated with epigenetic drift would be at the origin of organ dysfunction because of an increase in phenotypic variation among cells, ultimately leading to cell death and organ failure through a loss of coordination in cellular functions, and eventually to cancerization. We propose mechanistic research perspectives to corroborate this hypothesis and explore its evolutionary consequences, highlighting a positive correlation between the median age of mass loss onset (a proxy for the onset of organ aging) and the median age at cancer diagnosis.

中文翻译：

组织破坏诱导的细胞随机性和表观遗传漂移：衰老和癌症的共同起源？

与年龄相关和癌症相关的表观基因组修饰与增强的细胞间基因表达变异性有关，其特征是细胞随机性增加。由于在细胞分化过程中通过直接或远程细胞相互作用获得的表观遗传和表型稳定性似乎大大降低了基因表达变异性，因此我们提出了衰老和癌症的共同起源，即未能通过细胞 - 细胞控制细胞随机性。相互作用。与表观遗传漂移相关的组织破坏诱导的细胞随机性可能是器官功能障碍的根源，因为细胞之间的表型变异增加，最终导致细胞死亡和器官功能衰竭，最终导致细胞功能失调，并最终导致癌变.

更新日期：2020-12-22

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