Skip to main content
. Author manuscript; available in PMC: 2017 Jan 1.
Published in final edited form as: Biochim Biophys Acta. 2015 Oct 8;1865(1):14–22. doi: 10.1016/j.bbcan.2015.10.001

Figure 2. Senescence-inflammatory response in tumor stroma.

Figure 2

A. In a diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC) model, p53-dependent, senescent hepatic stellate cells promote the enrichment of M1-polarized macrophages. M1 macrophages limit the proliferation of initiated epithelial cells and consequently restrict HCC development.

B. A DMBA (7,12-dimethylbenz(a)anthracene)-initiated model of HCC demonstrated that livers of obese mice were predisposed to tumor development via DCA (deoxycholic acid)-induced senescent hepatic stellate cells. DCA was produced by the gut microbiota and resulted in increased senescence in the liver. The senescent stellate cells promoted tumorigenesis by the secretion of SASP factors.