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Escape cancer, but age sooner? The dark side of the tumor suppressing process
Date:12/1/2008

Cells shut down and stop dividing when their DNA is damaged, in a process known as cellular senescence, so as to prevent damaged DNA from leading to unregulated cell division and therefore cancer. However, a new study, published in this week's issue of PLoS Biology, has found that when these cells shut down they also spew proteins into their surrounding environment. This causes inflammation and sets up conditions that support the development of age-related diseases including, ironically, cancer. The new research includes the first comprehensive molecular description of a paradoxical process that prevents cancer in younger people, but promotes age-related cancers and other maladies later in life.

"We provide for the first time a broad molecular description of how this well known mechanism for cancer prevention drives aging and age-related disease by changing the local tissue environment," said Judith Campisi, PhD, lead author of the study, who is a Faculty Member of the Buck Institute for Age Research and also Senior Scientist at Lawrence Berkeley National Laboratory.

The study shows that the senescent cells secrete inflammatory, growth-stimulating, immunomodulatory, and other proteins that dramatically change the tissue microenvironment, both in cells grown in the lab and in people undergoing chemotherapy, which can cause DNA damage.

The study also showed that normal cells that acquire a highly active, mutant version of a cancer-promoting protein known as Ras secrete higher levels of the tissue-altering molecules, as do cells that lose functions of the tumor suppressor protein p53. The study therefore explains why the presence of senescent cells can promote the growth and aggressiveness of nearby precancerous or cancer cells, and further defines a new mechanism by which precancerous or cancer cells that have lost the p53 tumor suppressor, or gained an oncogene such as Ras, promote cancer so efficiently.

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Contact: Sally Hubbard
press@plos.org
Public Library of Science
Source:Eurekalert

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