{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Luo X"],"funding":["NIDDK NIH HHS","NCI NIH HHS","National Institutes of Health","National Research Foundation of Korea","Cholangiocarcinoma Foundation"],"pagination":["1411-1428"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9075007"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["74(3)"],"pubmed_abstract":["<h4>Background and aims</h4>Existing therapeutic approaches to treat cholangiocarcinoma (CCA) have limited effectiveness, prompting further study to develop therapies for CCA. We report a mechanistic role for the heparan sulfate editing enzyme sulfatase 2 (SULF2) in CCA pathogenesis.<h4>Approach and results</h4>In silico analysis revealed elevated SULF2 expression in human CCA samples, occurring partly through gain of SULF2 copy number. We examined the effects of knockdown or overexpression of SULF2 on tumor growth, chemoresistance, and signaling pathway activity in human CCA cell lines in vitro. Up-regulation of SULF2 in CCA leads to increased platelet-derived growth factor receptor beta (PDGFRβ)-Yes-associated protein (YAP) signaling activity, promoting tumor growth and chemotherapy resi"],"journal":["Hepatology (Baltimore, Md.)"],"pubmed_title":["Sulfatase 2 (SULF2) Monoclonal Antibody 5D5 Suppresses Human Cholangiocarcinoma Xenograft Growth Through Regulation of a SULF2-Platelet-Derived Growth Factor Receptor Beta-Yes-Associated Protein Signaling Axis."],"pmcid":["PMC9075007"],"funding_grant_id":["CA128633","R01 CA165076","R21 CA128633","P30 CA015083","P50 CA210964","P30 DK084567","2018R1C1B3004435","CA165076"],"pubmed_authors":["Lemjabbar-Alaoui H","Rosen SD","Torbenson MS","Singer MS","Ahn KS","Smoot R","Campbell NA","Luo X","He L","O'Brien DR","Roberts LR"],"additional_accession":[]},"is_claimable":false,"name":"Sulfatase 2 (SULF2) Monoclonal Antibody 5D5 Suppresses Human Cholangiocarcinoma Xenograft Growth Through Regulation of a SULF2-Platelet-Derived Growth Factor Receptor Beta-Yes-Associated Protein Signaling Axis.","description":"<h4>Background and aims</h4>Existing therapeutic approaches to treat cholangiocarcinoma (CCA) have limited effectiveness, prompting further study to develop therapies for CCA. We report a mechanistic role for the heparan sulfate editing enzyme sulfatase 2 (SULF2) in CCA pathogenesis.<h4>Approach and results</h4>In silico analysis revealed elevated SULF2 expression in human CCA samples, occurring partly through gain of SULF2 copy number. We examined the effects of knockdown or overexpression of SULF2 on tumor growth, chemoresistance, and signaling pathway activity in human CCA cell lines in vitro. Up-regulation of SULF2 in CCA leads to increased platelet-derived growth factor receptor beta (PDGFRβ)-Yes-associated protein (YAP) signaling activity, promoting tumor growth and chemotherapy resi","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-05-31T16:02:54.245Z","creation":"2025-02-19T01:28:02.483Z"},"accession":"S-EPMC9075007","cross_references":{"pubmed":["33735525"],"doi":["10.1002/hep.31817"]}}