| Literature DB >> 30392787 |
Qiaoting Deng1, Yan Geng2, Liying Zhao3, Ru Li4, Zhigao Zhang4, Kun Li4, Rongliang Liang5, Xiangyang Shao4, Maoliang Huang6, Daming Zuo7, Yingsong Wu8, Qiang Ma9.
Abstract
Inflammation and immunity are important determinants of cancer initiation, promotion, and progression to cancer equilibrium or suppression. The NOD-like receptor family pyrin domain containing 3 (NLRP3) is an oligomeric intracellular immune receptor, and the main component of inflammasome. As a widely distributed effector of innate immunity, NLRP3 inflammasome affects development of many cancer types, but its exact role in colorectal cancer (CRC) is controversial. We found that cells with the macrophage (MΦ) marker CD68 and strong NLRP3 expression densely surrounded CRC tissue. The NLRP3 inflammasome was activated in MΦs by MΦ-CRC cell crosstalk; it resulted in faster migration of CRC cells, whereas blocking NLRP3 signaling suppressed CRC cell migration in vitro, and metastatic ability in vivo. NLRP3 signaling activation in MΦs can contribute to CRC cell migration and invasion.Entities:
Keywords: Colorectal cancer; Liver metastasis; Macrophage; NLRP3 inflammasome; Tumor microenvironment
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Year: 2018 PMID: 30392787 DOI: 10.1016/j.canlet.2018.10.030
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679