Cellular Senescence as a Failed Anti-Cancer Strategy

The evolution of multi-cellular life is in essence the story of a tooth and nail struggle with cancer, one that continues even now. Complex structure, regeneration, and growth are all required in higher forms of life, but that combination means that any sort of sustained breakdown in control over cell proliferation tends to be fatal because it disrupts necessary structures. Multiple layered systems, within cells and outside them, have evolved to try to block damaged cells from uncontrolled proliferation, ranging from tumor suppressor genes to the surveillance of the immune system and its destruction of potentially cancerous cells. Cellular senescence is one of these strategies, and like all of them, it is only somewhat successful. With only a few rare exceptions, evolution has curbed cancer risk to the minimum degree needed for a species to survive, no more than that. Cellular senescence is, of course, one of the causes of aging. Cells become senescence in response to damage, a toxic environment, or at the end of their replicative life span, and near all destroy themselves or are destroyed by the immune system. Enough linger to cause problems, however, producing the senescence-associated secretory phenotype (SASP) that disrupts tissue structure and function. Cellular senescence is an anti-cancer strategy because senescence locks down a cell to prevent replication - so it should function to remove the most at-risk cells before they can run off the rails. Indeed, this wo...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs