Senescence is a double-edged sword that can function in opposite directions. It is a potential mechanism for a cell to avoid malignant transformation. However, senescence can also promote cancer development by altering the cellular microenvironment through a senescence-associated secretory phenotype (SASP). At least, three types of cellular stress such as activation of oncogenes, loss of tumor suppressor genes, and chemo/radiotherapy can induce cell senescence. Oncogene-induced senescence can be intertwiningly associated with the replicative senescence. Early-stage senescence may protect cell from transformation, while prolonged senescence often promotes cancer development. This review will focus on the characteristics of senescence, discuss the regulation of senescence during cancer development, and highlight the complexity of senescence that makes cancer treatment challenging.
