Abstract
Cellular senescence is defined as the physiological program of terminal growth arrest, which can be triggered by various endogenous or exogenous stress signals. Cellular senescence can be induced in response to oncogenic activation and acts as a barrier to tumorigenesis. Moreover, tumor cells can undergo senescence when exposed to chemotherapeutic agents. In addition to suppressing tumorigenesis, senescent cells remain metabolically active and may contribute to tumor formation and to therapy resistance. In the current review, we discuss the molecular regulation of cellular senescence, the potential implications of senescence in human cancers, and the possibility of exploiting cellular senescence for the treatment of cancers.
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