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Cellular senescence a double-edged sword
Date:12/3/2008

SASP, and determined that it occurs not only in cultured cells, but also in vivo in response to DNA damage.

"We showed that SASP develops slowly over several days and only after DNA damage of sufficient magnitude to induce senescence," Campisi said. "All SASP features high levels of secreted inflammatory cytokines, immune modulators, and growth factors, which are associated with inflammation and malignancy."

Oncogenes and Tumor Suppressors

While Campisi and her co-authors found that secretion of SASP was common to all senescent cells, there were distinct quantitative and qualitative differences among the different cell strains and lines. This paved the way for additional findings concerning genes that encode tumor promoting proteins (oncogenes) and those that encode tumor-suppressing proteins. For example, normal cells that acquired a highly active version of the RAS oncogene became senescent and secreted higher levels of SASP components. This very intense SASP also happened when cells lost the functions of the p53 tumor suppressor gene.

"Our findings help explain why senescent cells promote the growth and aggressiveness of nearby pre-cancerous or cancer cells, and define a new mechanism by which pre-cancerous or cancer cells that have lost the p53 tumor suppressor gene, or gained an oncogene such as RAS, promote cancer so efficiently," Campisi said.

These findings also raise a cautionary note with regards to the use of DNA-damaging chemotherapy on patients under the age of 50. Such treatments are aimed at cells that are undergoing rapid division but impact neighboring normal cells as well. As the findings of Campisi and her co-authors show, sufficient DNA damage forces both cancerous and normal cells into senescence, releasing SASP components. The resulting inflammation of neighboring cells and tissue would explain why so many patients receiving chemotherapy experience flu-like symptoms during treatments. Such
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Contact: Lynn Yarris
lcyarris@lbl.gov
510-486-5375
DOE/Lawrence Berkeley National Laboratory
Source:Eurekalert  

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