{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Huang H"],"funding":["National Cancer Institute","NCI NIH HHS","National Institute of General Medical Sciences","NIGMS NIH HHS"],"pagination":["23208-23223"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5087738"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["291(44)"],"pubmed_abstract":["Pancreatic ductal adenocarcinomas are highly malignant cancers characterized by extensive invasion into surrounding tissues, metastasis to distant organs, and a limited response to therapy. A main feature of pancreatic ductal adenocarcinomas is desmoplasia, which leads to extensive deposition of collagen I. We have demonstrated that collagen I can induce epithelial-mesenchymal transition (EMT) in pancreatic cancer cells. A hallmark of EMT is an increase in the expression of the mesenchymal cadherin N-cadherin. Previously we showed up-regulation of N-cadherin promotes tumor cell invasion and that collagen I-induced EMT is mediated by two collagen receptors, α2β1-integrin and discoidin domain receptor 1 (DDR1). DDR1 is a receptor-tyrosine kinase widely expressed during embryonic development "],"journal":["The Journal of biological chemistry"],"pubmed_title":["Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1."],"pmcid":["PMC5087738"],"funding_grant_id":["P30 CA036727","U01 CA111294","R01GM051188","P50 CA127297","P30 GM106397","U01CA111294","U54CA163120","R21CA137401","U54 CA163120","R21 CA137401","P30CA036727","R01 GM051188","P30GM1063970","P50CA127297"],"pubmed_authors":["Lazenby AJ","Wheelock MJ","Huang H","Saowapa J","Chaika N","Johnson KR","Ding K","Svoboda RA"],"additional_accession":[]},"is_claimable":false,"name":"Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1.","description":"Pancreatic ductal adenocarcinomas are highly malignant cancers characterized by extensive invasion into surrounding tissues, metastasis to distant organs, and a limited response to therapy. A main feature of pancreatic ductal adenocarcinomas is desmoplasia, which leads to extensive deposition of collagen I. We have demonstrated that collagen I can induce epithelial-mesenchymal transition (EMT) in pancreatic cancer cells. A hallmark of EMT is an increase in the expression of the mesenchymal cadherin N-cadherin. Previously we showed up-regulation of N-cadherin promotes tumor cell invasion and that collagen I-induced EMT is mediated by two collagen receptors, α2β1-integrin and discoidin domain receptor 1 (DDR1). DDR1 is a receptor-tyrosine kinase widely expressed during embryonic development ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Oct","modification":"2025-04-04T14:57:46.158Z","creation":"2019-03-27T02:27:53Z"},"accession":"S-EPMC5087738","cross_references":{"pubmed":["27605668"],"doi":["10.1074/jbc.m116.740605","10.1074/jbc.M116.740605"]}}