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Collagen type I-induced Smad-interacting protein 1 expression downregulates E-cadherin in pancreatic cancer
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Collagen type I-induced Smad-interacting protein 1 expression downregulates E-cadherin in pancreatic cancer
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Journal Article
Collagen type I-induced Smad-interacting protein 1 expression downregulates E-cadherin in pancreatic cancer
2007
Overview
Pancreatic cancer is a devastating disease with poor prognosis. Production of large quantities of extracellular matrix and early metastasis are characteristics of this disease. One important step in the development of various cancers is the loss of E-cadherin gene expression or inactivation of E-cadherin mediated cell–cell adhesion. It has been shown that collagen type I promotes downregulation of E-cadherin expression, which correlates with enhanced cell migration and invasiveness. In this context, we elucidated the role of Smad-interacting protein 1 (SIP1), which has been discussed as a negative regulator of E-cadherin gene expression. We demonstrate that SIP1 upregulation shows an inverse relationship with E-cadherin in advanced pancreatic tumour stages. In Panc-1 cells, SIP1 expression can be induced by exposure to collagen type I in a src-dependent manner. In addition, overexpression of SIP1 reduces E-cadherin mRNA and protein levels. Taken together, these results suggest that SIP1 is involved in the progression of pancreatic cancer and plays a role in mediating signal transduction from collagen type I to downregulate E-cadherin expression.
Publisher
Nature Publishing Group UK,Nature Publishing,Nature Publishing Group
Subject
/ Biological and medical sciences
/ Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
/ Cellular signal transduction
/ Collagen
/ Fundamental and applied biological sciences. Psychology
/ Gastroenterology. Liver. Pancreas. Abdomen
/ Gene Expression Regulation, Neoplastic
/ Homeodomain Proteins - genetics
/ Humans
/ Liver. Biliary tract. Portal circulation. Exocrine pancreas
/ Medicine
/ Molecular and cellular biology
/ Oncology
/ Pancreatic Neoplasms - genetics
/ Proteins
/ Repressor Proteins - genetics
/ Tumors
