| Literature DB >> 27855278 |
Chiara Birtolo1, Hung Pham2, Susan Morvaridi2, Chintan Chheda2, Vay Liang W Go3, Andrzej Ptasznik2, Mouad Edderkaoui2, Michael H Weisman2, Erika Noss4, Michael B Brenner4, Brent Larson5, Maha Guindi5, Qiang Wang6, Stephen J Pandol7.
Abstract
Chronic pancreatitis is a prominent risk factor for the development of pancreatic ductal adenocarcinoma. In both conditions, the activation of myofibroblast-like pancreatic stellate cells (PSCs) plays a predominant role in the formation of desmoplastic reaction through the synthesis of connective tissue and extracellular matrix, inducing local pancreatic fibrosis and an inflammatory response. Yet the signaling events involved in chronic pancreatitis and pancreatic cancer progression and metastasis remain poorly defined. Cadherin-11 (Cad-11, also known as OB cadherin or CDH11) is a cell-to-cell adhesion molecule implicated in many biological functions, including tissue morphogenesis and architecture, extracellular matrix-mediated tissue remodeling, cytoskeletal organization, epithelial-to-mesenchymal transition, and cellular migration. In this study, we show that, in human chronic pancreatitis and pancreatic cancer tissues, Cad-11 expression was significantly increased in PSCs and pancreatic cancer cells. In particular, an increased expression of Cad-11 can be detected on the plasma membrane of activated PSCs isolated from chronic pancreatitis tissues and in pancreatic cancer cells metastasized to the liver. Moreover, knockdown of Cad-11 in cancer cells reduced pancreatic cancer cell migration. Taken together, our data underline the potential role of Cad-11 in PSC activation and pancreatic cancer metastasis.Entities:
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Year: 2016 PMID： 27855278 PMCID： PMC5225304 DOI： 10.1016/j.ajpath.2016.09.012
Source DB: PubMed Journal: Am J Pathol ISSN： 0002-9440 Impact factor: 5.770