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. 2014 Nov 11;1(4):e969167.
doi: 10.4161/23723548.2014.969167. eCollection 2014 Oct-Dec.

SIN3B, the SASP, and pancreatic cancer

David J Cantor  1 , Gregory David  1
Affiliations

SIN3B, the SASP, and pancreatic cancer

David J Cantor et al. Mol Cell Oncol. .

Abstract

Cellular senescence is classically considered a tumor suppressive mechanism. In addition to having stably exited the cell cycle, senescent cells secrete inflammatory factors. We recently demonstrated that senescence correlates with accelerated cancer progression in a mouse model of pancreatic ductal adenocarcinoma. Here, we discuss the implications of this study.

Keywords: IL-1α; SASP; Sin3; pancreatic ductal adenocarcinoma; senescence.

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Figures

Figure 1.
Figure 1.
Senescence-associated cytokines establish an inflammatory microenvironment and promote cancer progression. Upon oncogene activation cells become senescent. The senescent cells produce and secrete the senescence-associated secretory phenotype (SASP), which reinforces senescence within the lesion and recruits immune cells to the surrounding tissue. The immune cells, along with the SASP, generate an inflammatory microenvironment, which in certain contexts fuels cancer progression.
See this image and copyright information in PMC

References

    1. Hezel A, Kimmelman A, Stanger B, Bardeesy N, DePinho R. Genetics and biology of pancreatic ductal adenocarcinoma. Genes Dev 2006; 20:1218-49; PMID:16702400; http://dx.doi.org/ 10.1101/gad.1415606 - DOI - PubMed
    1. Caldwell ME, DeNicola GM, Martins CP, Jacobetz MA. Cellular features of senescence during the evolution of human and murine ductal pancreatic cancer. Oncogene 2012; 31(12):1599-1608; PMID:21860420; http://dx.doi.org/ 10.1038/onc.2011.350 - DOI - PMC - PubMed
    1. Pérez-Mancera PA, Young AR, Narita M. Inside and out: the activities of senescence in cancer. Nat Rev Cancer 2014; 14(8):547-58; PMID:25030953; http://dx.doi.org/ 10.1038/nrc3773 - DOI - PubMed
    1. Grandinetti KB, Jelinic P, DiMauro T, Pellegrino J, Fernández Rodríguez R, Finnerty PM, Ruoff R, Bardeesy N, Logan SK, David G. Sin3B expression is required for cellular senescence and is up-regulated upon oncogenic stress. Cancer Res 2009; 69:6430-7; PMID:19654306; http://dx.doi.org/ 10.1158/0008-5472.CAN-09-0537 - DOI - PMC - PubMed
    1. Rielland M, Cantor DJ, Graveline R, Hajdu C, Mara L, Diaz B de D, Miller G, David G. Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression. J Clin Invest 2014; 124:2125-35; PMID:24691445; http://dx.doi.org/ 10.1172/JCI72619 - DOI - PMC - PubMed

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