title: Cellular senescence: a double-edged sword in the fight against cancer.
abstract: Over the last few decades, it has become apparent that oncogenic proliferative signals are coupled to a variety of growth inhibitory responses, such as the induction of apoptotic cell death or irreversible cell cycle arrest known as 'cellular senescence'. Thus, both apoptosis and cellular senescence are thought to act as important tumor suppression mechanisms. Unlike apoptotic cells, however, senescent cells remain viable for long periods of time and accumulate with increasing age in various organs and tissues. Moreover, recent studies reveal that although cellular senescence initially functions as a tumor suppressive process, it may eventually exhibit tumor-promoting effects. Therefore, it is conceivable that accumulation of senescent cells during the ageing process in vivo may contribute to the age-related increase in cancer incidence. In this review, we provide an update and perspective on recent advances made in understanding the deleterious side effects of cellular senescence.
authors.affiliation: Division of Cancer Biology, Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Ohtani
authors.forename: Akiko
authors.initials: A
authors.lastname: Takahashi
authors.forename: David J
authors.initials: DJ
authors.lastname: Mann
authors.forename: Eiji
authors.initials: E
authors.lastname: Hara
mesh_terms: D000818:Animals; D017209:Apoptosis; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D016922:Cellular Senescence; D004249:DNA Damage; D044127:Epigenesis, Genetic; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D007249:Inflammation; D008954:Models, Biological; D009369:Neoplasms / Q000378:metabolism / Q000517:prevention & control* / Q000628:therapy*; D018384:Oxidative Stress