Senescent cells as a source of inflammatory factors for tumor progression

By Albert R. Davalos, Jean-Philippe Coppé, J. Campisi, P. Desprez. Cancer Metastasis Review, 2010

624 citations recorded by the source corpus.

Cellular senescence, which is associated with aging, is a process by which cells enter a state of permanent cell cycle arrest, therefore constituting a potent tumor suppressive mechanism. Recent studies show that, despite the beneficial effects of cellular senescence, senescent cells can also exert harmful effects on the tissue microenvironment. The most significant of these effects is the acquisition of a senescent-associated secretory phenotype (SASP), which entails a striking increase in the secretion of pro-inflammatory cytokines. Here, we summarize our knowledge of the SASP and the impact it has on tissue microenvironments and ability to stimulate tumor progression.

Subfields: Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/f84f57cf4d4862cd83a1b680afb9b85cf0ba9d15

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. Campisi
2. Adam Freund
3. S. Grivennikov
4. C. Patil
5. F. Greten
6. M. Karin
7. M. Demaria
8. Y. Fouad

In Physiology

1. J. Campisi
2. Adam Freund
3. C. Patil
4. M. Demaria
5. Jesús Gil
6. J. Kirkland
7. Jan M. van Deursen
8. T. Tchkonia

Citations in the corpus

• Aging, Cellular Senescence, and Cancer (2012, background): “Of particular relevance to the role of cellular senescence in aging and age-related disease, many SASP components directly or indirectly promote inflammation (59, 92, 93, 107, 108).”
• Inflammation and Cancer: Triggers, Mechanisms and Consequences (2019, background): “Moreover, K-Rras activation enhances production of cytokines and chemokines that belong to “senescenceassociated secretory phenotype” (Davalos et al., 2010), including IL-1α, IL-1β, CCL2 and CXCL1.”
• p38MAPK is a novel DNA damage response‐independent regulator of the senescence‐associated secretory phenotype (2011, background): “…of the lowaffinity sites, making both p38MAPK and the DDR necessary for NF-kB activity. p38MAPK was crucial for the expression of many SASP cytokines and chemokines, which are largely pro-inflammatory and pro-carcinogenic (Davalos et al, 2010; Freund et al, 2010; Coppe et al, 2010a).”
• Oxidative Stress, Prooxidants, and Antioxidants: The Interplay (2014, background): “These factors are also required for the membrane degradation, invasion of neighboring tissues, and migration of tumor cells through vasculature and lymphatic channels for metastasis [135–137].”