{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360021390740411264.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1016/j.canlet.2023.216116"}},{"identifier":{"@type":"URI","@value":"https://api.elsevier.com/content/article/PII:S0304383523000678?httpAccept=text/xml"}},{"identifier":{"@type":"URI","@value":"https://api.elsevier.com/content/article/PII:S0304383523000678?httpAccept=text/plain"}},{"identifier":{"@type":"PMID","@value":"36878307"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"MUC1-C is necessary for SHP2 activation and BRAF inhibitor resistance in BRAF(V600E) mutant colorectal cancer"}],"description":[{"notation":[{"@value":"Colorectal cancers (CRCs) harboring the BRAF(V600E) mutation are associated with aggressive disease and resistance to BRAF inhibitors by feedback activation of the receptor tyrosine kinase (RTK)→RAS→MAPK pathway. The oncogenic MUC1-C protein promotes progression of colitis to CRC; whereas there is no known involvement of MUC1-C in BRAF(V600E) CRCs. The present work demonstrates that MUC1 expression is significantly upregulated in BRAF(V600E) vs wild-type CRCs. We show that BRAF(V600E) CRC cells are dependent on MUC1-C for proliferation and BRAF inhibitor (BRAFi) resistance. Mechanistically, MUC1-C integrates induction of MYC in driving cell cycle progression with activation of the SHP2 phosphotyrosine phosphatase, which enhances RTK-mediated RAS→ERK signaling. We demonstrate that targeting MUC1-C genetically and pharmacologically suppresses (i) activation of MYC, (ii) induction of the NOTCH1 stemness factor, and (iii) the capacity for self-renewal. We also show that MUC1-C associates with SHP2 and is required for SHP2 activation in driving BRAFi-induced feedback of ERK signaling. In this way, targeting MUC1-C in BRAFi-resistant BRAF(V600E) CRC tumors inhibits growth and sensitizes to BRAF inhibition. These findings demonstrate that MUC1-C is a target for the treatment of BRAF(V600E) CRCs and for reversing their resistance to BRAF inhibitors by suppressing the feedback MAPK pathway."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380021390740411294","@type":"Researcher","foaf:name":[{"@value":"Yoshihiro Morimoto"}]},{"@id":"https://cir.nii.ac.jp/crid/1420577199223804288","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"60608967"},{"@type":"NRID","@value":"1000060608967"},{"@type":"NRID","@value":"9000017288575"}],"foaf:name":[{"@value":"Nami Yamashita"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411148","@type":"Researcher","foaf:name":[{"@value":"Haruka Hirose"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411302","@type":"Researcher","foaf:name":[{"@value":"Atsushi Fushimi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411285","@type":"Researcher","foaf:name":[{"@value":"Naoki Haratake"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411272","@type":"Researcher","foaf:name":[{"@value":"Tatsuaki Daimon"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411274","@type":"Researcher","foaf:name":[{"@value":"Atrayee Bhattacharya"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411012","@type":"Researcher","foaf:name":[{"@value":"Rehan Ahmad"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411296","@type":"Researcher","foaf:name":[{"@value":"Yozo Suzuki"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411147","@type":"Researcher","foaf:name":[{"@value":"Hidekazu Takahashi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021390740411269","@type":"Researcher","foaf:name":[{"@value":"Donald W. Kufe"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"03043835"}],"prism:publicationName":[{"@value":"Cancer Letters"}],"dc:publisher":[{"@value":"Elsevier 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Tumor"},{"@id":"https://cir.nii.ac.jp/all?q=Mucin-1","dc:title":"Mucin-1"},{"@id":"https://cir.nii.ac.jp/all?q=Mutation","dc:title":"Mutation"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Receptor%20Protein-Tyrosine%20Kinases","dc:title":"Receptor Protein-Tyrosine Kinases"},{"@id":"https://cir.nii.ac.jp/all?q=Colorectal%20Neoplasms","dc:title":"Colorectal Neoplasms"},{"@id":"https://cir.nii.ac.jp/all?q=Protein%20Kinase%20Inhibitors","dc:title":"Protein Kinase Inhibitors"},{"@id":"https://cir.nii.ac.jp/all?q=Signal%20Transduction","dc:title":"Signal 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