The effect on proliferation may be an unwanted byproduct of the senescence expression program, which includes increased levels of an odd mixture of molecules. Only a few of these molecules are involved in cell cycle arrest, but a number may promote epithelial proliferation.
Campisi says that the expression mix may have arisen when evolution co-opted an existing program involved in wound healing to shut down the cell division of senescent fibroblasts. Wounding eventually blocks fibroblast division, as is required during senescence, but it also results in production of matrix remodeling enzymes (to clear up the mess), cytokines (to recruit macrophages), and epithelial growth factors (to close the wound). These same factors, produced in increasing amounts by increasing numbers of senescent cells, may promote the development of epithelial cancers, which constitute the vast majority of late-onset cancers in humans. ▪