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

细胞衰老是一种不可逆的细胞增殖停滞，由致癌冲动引起，如致癌基因激活，产生有害的DNA损伤，被认为是一种重要的故障安全机制。最近有报道称，衰老细胞产生多种类型的分泌蛋白，包括炎症细胞因子和趋化因子。在这项研究中，我们研究了这种与衰老相关的分泌蛋白是否促进了癌症的进展。我们发现衰老的肝星状细胞（hsc）在肥胖诱导的肝细胞癌组织中形成肿瘤微环境。此外，我们还阐明了造血干细胞衰老的机制以及哪些信号参与分泌蛋白的产生。

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.