{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(46)"],"submitter":["Cheng W"],"pubmed_abstract":["Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is a major cause of cancer-related death worldwide. Previously, we demonstrated that glypican-3 (GPC3) is highly expressed in HCC, and that GPC3 induces oncogenicity and promotes the growth of cancer cells through IGF-1 receptor (IGF-1R). In the present study, we investigated the mechanisms of GPC3-mediated enhancement of IGF-1R signaling. We demonstrated that GPC3 decreased IGF-1-induced IGF-1R ubiquitination and degradation and increased c-Myc protein levels. GPC3 bound to Grb10, a mediator of ligand-induced receptor ubiquitination, and the overexpression of Grb10 blocked GPC3-enhanced IGF-1-induced ERK phosphorylation. GPC3 promoted the growth of NIH3T3 and PLC-PRF-5 cells in serum-free medium but did not pro"],"journal":["Oncotarget"],"pagination":["80429-80442"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5655209"],"repository":["biostudies-literature"],"pubmed_title":["Glypican-3 induces oncogenicity by preventing IGF-1R degradation, a process that can be blocked by Grb10."],"pmcid":["PMC5655209"],"pubmed_authors":["Hwu WL","Chao HM","Jeng YM","Hsu HC","Lee YM","Huang PC","Cheng W","Pan HW"],"additional_accession":[]},"is_claimable":false,"name":"Glypican-3 induces oncogenicity by preventing IGF-1R degradation, a process that can be blocked by Grb10.","description":"Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is a major cause of cancer-related death worldwide. Previously, we demonstrated that glypican-3 (GPC3) is highly expressed in HCC, and that GPC3 induces oncogenicity and promotes the growth of cancer cells through IGF-1 receptor (IGF-1R). In the present study, we investigated the mechanisms of GPC3-mediated enhancement of IGF-1R signaling. We demonstrated that GPC3 decreased IGF-1-induced IGF-1R ubiquitination and degradation and increased c-Myc protein levels. GPC3 bound to Grb10, a mediator of ligand-induced receptor ubiquitination, and the overexpression of Grb10 blocked GPC3-enhanced IGF-1-induced ERK phosphorylation. GPC3 promoted the growth of NIH3T3 and PLC-PRF-5 cells in serum-free medium but did not pro","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2025-04-20T00:21:14.602Z","creation":"2019-03-27T02:59:48Z"},"accession":"S-EPMC5655209","cross_references":{"pubmed":["29113314"],"doi":["10.18632/oncotarget.19035"]}}