Year: 2019
Type: article
Abstract: The Muc-1 oncoprotein is a tumor-associated mucin often overexpressed in pancreatic cancer. We report that knockout of Muc-1 reduced the degree of pancreatic inflammation that resulted from infection with Coxsackievirus B3 (CVB3) in a mouse model. CVB3-infected Muc-1-deficient (Muc-1KO) mice had significantly reduced infiltration of macrophages into the murine pancreas. We found that Muc-1 signaling through NF-κB increased expression of ICAM-1, a pro-inflammatory mediator that recruits macrophages. Further investigation revealed that bone marrow derived macrophages (BMDM) from the Muc-1KOmice exhibited defective migration properties, in part due to low expression of the C-C motif chemokine receptor (CCR2) and the integrin Very Late Antigen 4 (VLA-4). The results presented here provide novel insight into the role of Muc-1 in regulating the inflammatory response and the cellular microenvironment in pancreatitis.
Source: Scientific Reports
Institutions: Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Mayo Clinic, Mayo Clinic in Florida, Mayo Clinic Comprehensive Cancer Center (Florida), The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $1,790
Awards: G1035894591, G1041813518, G129289406, PDG Links Stem Cell Niche to Pancreatic Epithelial Renewal, Repair and Cancer, G2220859824, G2744939468, G4749921586, G6171233599, SPORE in Pancreatic Cancer, PKD1 signaling in the initiation of pancreatic cancer, G7204339488, Immunometabolism in microbial sepsis , G9000153906, G9000160336, G9000207739, G9000298788, Buffett Cancer Center Support Grant, G911360726, G93971369
OpenAlex ID: W2963878884