{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Probst OC"],"funding":["Austrian Science Fund FWF"],"pagination":["91-9"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3632087"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["451(1)"],"pubmed_abstract":["The M6P (mannose 6-phosphate)/IGF2R (insulin-like growth factor II receptor) interacts with a variety of factors that impinge on tumour invasion and metastasis. It has been shown that expression of wild-type M6P/IGF2R reduces the tumorigenic and invasive properties of receptor-deficient SCC-VII squamous cell carcinoma cells. We have now used mutant forms of M6P/IGF2R to assess the relevance of the different ligand-binding sites of the receptor for its biological activities in this cellular system. The results of the present study demonstrate that M6P/IGF2R does not require a functional binding site for insulin-like growth factor II for inhibition of anchorage-independent growth and matrix invasion by SCC-VII cells. In contrast, the simultaneous mutation of both M6P-binding sites is suffici"],"journal":["The Biochemical journal"],"pubmed_title":["The mannose 6-phosphate-binding sites of M6P/IGF2R determine its capacity to suppress matrix invasion by squamous cell carcinoma cells."],"pmcid":["PMC3632087"],"funding_grant_id":["P 20918"],"pubmed_authors":["Puxbaum V","Karayel E","Nimmerfall E","Schida N","Hehenberger E","Probst OC","Mach L"],"additional_accession":[]},"is_claimable":false,"name":"The mannose 6-phosphate-binding sites of M6P/IGF2R determine its capacity to suppress matrix invasion by squamous cell carcinoma cells.","description":"The M6P (mannose 6-phosphate)/IGF2R (insulin-like growth factor II receptor) interacts with a variety of factors that impinge on tumour invasion and metastasis. It has been shown that expression of wild-type M6P/IGF2R reduces the tumorigenic and invasive properties of receptor-deficient SCC-VII squamous cell carcinoma cells. We have now used mutant forms of M6P/IGF2R to assess the relevance of the different ligand-binding sites of the receptor for its biological activities in this cellular system. The results of the present study demonstrate that M6P/IGF2R does not require a functional binding site for insulin-like growth factor II for inhibition of anchorage-independent growth and matrix invasion by SCC-VII cells. In contrast, the simultaneous mutation of both M6P-binding sites is suffici","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Apr","modification":"2025-04-26T15:31:36.046Z","creation":"2019-03-27T01:07:43Z"},"accession":"S-EPMC3632087","cross_references":{"pubmed":["23347038"],"doi":["10.1042/BJ20121422"]}}