The molecular mechanism of senescence-associated prolongation of inflammatory signaling and its effect on cancer micro-environments.

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Cellular senescence is an irreversible cell proliferation arrest provoked by oncogenic impulse such as oncogene activation that creates harmful DNA damage, and is recognized as an important fail-safe mechanism. Recently, it has been reported that senescent cells produce various types of secretory proteins including inflammatory cytokines and chemokines. In this study, we investigated whether this senescence-associated secretory proteins promote cancer progression. We found that senescent hepatic stellate cells (HSCs) form cancer micro-environment in obesity-induced hepatocellular carcinoma tissue. Moreover, we clarified the mechanism of how HSCs senesce and what signal is involved in the production of secretory proteins.