Shin Yoshimoto

TL;DR: It is shown that senescence-associated secretory phenotype (SASP) has crucial roles in promoting obesity-associated hepatocellular carcinoma (HCC) development in mice, and a similar pathway may contribute to at least certain aspects of obesity- associated HCC development in humans as well.

TL;DR: Results indicate that exosome secretion maintains cellular homeostasis by removing harmful cytoplasmic DNA from cells, and provide valuable new insights into the control of cellularHomeostasis.

TL;DR: It is shown that the hepatic translocation of obesity-induced lipoteichoic acid (LTA), a Gram-positive gut microbial component, promotes HCC development by creating a tumor-promoting microenvironment, and the importance of the gut-liver axis in obesity-associated HCC is shown.

TL;DR: It is shown that, in senescent cells, the DDR induces proteasomal degradation of G9a and GLP, major histone H3K9 mono- and dimethyltransferases, through Cdc14B- and p21(Waf1/Cip1)-dependent activation of APC/C(Cdh1) ubiquitin ligase, thereby causing a global decrease in H 3K9 dimethylation, an epigenetic mark for euchromatic

TL;DR: These findings establish an intrinsic cooperation between p16INK4a and p21Waf1/Cip1 in the onset of cellular senescence and tumor suppression in vivo.