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. 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 1. Senescence-inflammatory response in epithelium.

Figure 1

A. Oncogene-induced senescence (OIS) in hepatic tumor cells, through secretion of SASP-factor CCL2, stimulates natural killer (NK) cell-mediated anti-tumor immune responses.

B. Using a model of NrasG12V-driven, OIS, senescent premalignant hepatocytes stimulate immune surveillance by secretion of SASP factors. SASP factors results in the activation of CD4+, TH1 cells, which subsequently limit liver cancer development via macrophage/monocyte mediate clearance.

C. PTEN-loss induced senescent prostate tumor cells promote cancer progression by the SASP factor-mediated establishment of immunosuppressive inflammation. In this model, Jak2/Stat3 dependent SASP factor expression results in recruitment of CD11b+Gr-1+ myeloid cells which limit cytotoxic T cell (CTL) function and thus tumor growth is unrestrained.

D. In a model of colorectal cancer, a SASP related secretory profile, termed the senescence-associated inflammatory response (SIR), is secreted by stressed epithelial cells. The SIR promotes tumorigenesis following the loss of p53 expression. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) can reverse the tumor promoting effects of the SIR.