By secreting damaging molecules and cytokines, senescent cells can disrupt the surrounding tissue microenvironment. There are several lines of evidence supporting this conclusion. Cells from older people senesce after only a fraction of the cell divisions that fetal cells can undergo. Cells from people with genetic premature aging syndromes senesce prematurely, suggesting that the same genes regulate life span in the cell and the organism. There is another direct connection between cellular senescence, aging and mortality.
Most tumors contain cells that continue to divide beyond normal limits or indefinitely.
Tumor suppressor genes are thought to act in part by inducing cellular senescence, which puts a halt to cell division. This has led scientists to the intriguing hypothesis that cellular senescence evolved as a defense against cancer. In support of this theory, recent research shows that cells can respond to carcinogenic stimuli such as DNA damage and the activation of cancer-promoting genes by entering a senescent state. Rapid effective proteolysis is therefore an anti-aging mechanism. The double-edged sword of cellular senescence thereby consigns cells to mortality in order to protect them against cancer.