Senescent cells, albeit not proliferating, are metabolically and transcriptionally active, thereby capable of affecting their microenvironment, notably via the production of inflammatory mediators. These mediators maintain and propagate the senescence process to neighboring cells, and then recruit immune cells for clearing senescent cells. Among the inflammatory cues are molecules with pronounced tumor-controlling properties, both growth and invasion factors and inhibitory factors, working directly or via recruited immune cells. These senescence-inflammatory effects also prevail within tumors, mediated by the senescent tumor cells and the senescent tumor stroma. Here, we review the course and impact of senescence-associated inflammatory responses in aging and cancer. We propose that controlling senescence-associated inflammation by targeting specific inflammatory mediators may have a beneficial therapeutic effect in treatment of cancer and aging-related diseases.
Bibliographical noteFunding Information:
We thank Irit Snir-Alkalay and Adar Zinger for insightful comments on the manuscript. Work in our lab is supported by grants from Israel Science Foundation (ISF) - Centers of Excellence; the European Research Council within the FP-7 (294390 PICHO); The Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF); The I-CORE program of ISF (grant No 41/11) and Israel Cancer Research fund.
© 2015 Elsevier Ltd.