<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang H</submitter><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>23208-23223</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5087738</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>291(44)</volume><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 </pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1.</pubmed_title><pmcid>PMC5087738</pmcid><funding_grant_id>P30 CA036727</funding_grant_id><funding_grant_id>U01 CA111294</funding_grant_id><funding_grant_id>R01GM051188</funding_grant_id><funding_grant_id>P50 CA127297</funding_grant_id><funding_grant_id>P30 GM106397</funding_grant_id><funding_grant_id>U01CA111294</funding_grant_id><funding_grant_id>U54CA163120</funding_grant_id><funding_grant_id>R21CA137401</funding_grant_id><funding_grant_id>U54 CA163120</funding_grant_id><funding_grant_id>R21 CA137401</funding_grant_id><funding_grant_id>P30CA036727</funding_grant_id><funding_grant_id>R01 GM051188</funding_grant_id><funding_grant_id>P30GM1063970</funding_grant_id><funding_grant_id>P50CA127297</funding_grant_id><pubmed_authors>Lazenby AJ</pubmed_authors><pubmed_authors>Wheelock MJ</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Saowapa J</pubmed_authors><pubmed_authors>Chaika N</pubmed_authors><pubmed_authors>Johnson KR</pubmed_authors><pubmed_authors>Ding K</pubmed_authors><pubmed_authors>Svoboda RA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Up-regulation of N-cadherin by Collagen I-activated Discoidin Domain Receptor 1 in Pancreatic Cancer Requires the Adaptor Molecule Shc1.</name><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 </description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Oct</publication><modification>2025-04-04T14:57:46.158Z</modification><creation>2019-03-27T02:27:53Z</creation></dates><accession>S-EPMC5087738</accession><cross_references><pubmed>27605668</pubmed><doi>10.1074/jbc.m116.740605</doi><doi>10.1074/jbc.M116.740605</doi></cross_references></HashMap>