Cellular senescence is a form of irreversible arrest initially characterized as thestate attained at the end of a cell’s replicative lifespan. Subsequently, senescence has been linked with organismal aging and is suggested as a key driver of the aging process [1]. However,senescence can also be induced prematurely in response to active oncogenes and DNA damage. This oncogene-induced senescence (OIS) is a potent tumor suppressive mechanism in vivo, preventing the aberrant proliferation of initiated cells; and for a tumor to form, the cell must overcome senescence-imposed barriers. In addition, the reactivation ofsenescence within the tumor microenvironment, or in response to chemotherapy, can aid in the arrest of tumor growth and facilitate tumor clearance, highlighting its promise as a therapeutic mechanism [2]. In brief, senescence represents a critical focalpoint between cancer andaging, requiring that a precise balance be maintained to avoid predisposition toeither process. Consequently, understanding the molecular regulation of senescence is crucial to cancer treatment and anti-aging therapies.
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