[Senescence and Cancer]

Cells experiencing significant stress such as irreparable genomic damage enter a state called cellular senescence, where their cell cycle is irreversibly arrested. Originally, cellular senescence was thought to serve as a crucial mechanism for suppressing carcinogenesis by stopping the growth of abnormal cells that could potentially lead to cancer development. However, it has become evident that senescence induced by treatments such as chemotherapy can contribute to drug resistance in cancer by exhibiting resistance to cell death and allowing cancer cells to survive. Furthermore, senescent cells exhibit a property known as the senescence-associated secretory phenotype(SASP), where they release a variety of inflammatory molecules and growth factors. Through these SASP factors influencing the tumor microenvironment, senescent cells can be deeply involved in various cancer pathologies such as carcinogenesis and the acquisition of drug resistance. This article provides an overview of the multifaceted and complex interplay between cellular senescence and the initiation and progression of cancer.