作者: Véronique Bourdeau , Gerardo Ferbeyre
DOI: 10.1007/978-1-4419-1075-2_3
关键词: Downregulation and upregulation 、 Cell biology 、 Senescence 、 Kinase 、 Suppressor 、 Chemistry 、 Promyelocytic leukemia protein 、 DNA replication 、 DNA damage 、 Cyclin-dependent kinase
摘要: Oncogene-Induced Senescence (OIS) is a tumor suppressor mechanism that prevents the expansion of cells bearing activated oncogenes. Two major suppressors control OIS: p53 and Rb. These are not to regulate senescence by normal growth signals, but stress signals caused The activation oncogenes involves reactive oxygen species (oxidative stress), DNA replication damage response. Rb during OIS less understood, it Cyclin-Dependent Kinases (CDKs) inhibitors such as p21 p16INK4a or downregulation CDK4, due decrease in Myc functions. also controls formation heterochromatin senescent cells, this process has been linked p16INK4a, promyelocytic leukemia protein PML. occurs both rodents humans, its differ between these species. In rodents, can be inactivated disabling pathway. contrast, human organize Rb-independent senescence. initiated cell autonomous response oncogenes, secreted cytokines. mechanistic understanding suggests novel strategies treat cancers.