{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang B"],"funding":["NIDDK NIH HHS","NCI NIH HHS"],"pagination":["e00144"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10289747"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(7)"],"pubmed_abstract":["<h4>Background</h4>We established a novel diethylnitrosamine (DEN) -induced mouse model that reflected the progression of cholangiocarcinoma (CCA) from atypical cystic hyperplasia.<h4>Methods</h4>BALB/c mice were administered DEN by oral gavage. Cells isolated from livers were analyzed for expression of CSNK2A1, MAX and MAX-interacting proteins. Human CCA cell lines (MzChA-1, HuCCT1), normal human cholangiocyte (H69), human hepatic stellate cells (LX-2), macrophages (RAW 264.7), and primary hepatic cells were used for cellular and molecular biology assays.<h4>Results</h4>Expression of MAX, CSNK2A1, C-MYC, β-catenin, HMGB1, and IL-6 was upregulated in hepatic cells from CCA liver tissue. The half-life of MAX is higher in CCA cells, and this favors their proliferation. Overexpression of MAX "],"journal":["Hepatology communications"],"pubmed_title":["CSNK2A1-mediated MAX phosphorylation upregulates HMGB1 and IL-6 expression in cholangiocarcinoma progression."],"pmcid":["PMC10289747"],"funding_grant_id":["R01 DK123763","R01 CA172086","R01 DK107288"],"pubmed_authors":["Yang H","Fan W","Lu SC","Zhang J","Barbier-Torres L","Yang B","Liu T","Wang J","Steggerda J","Ramani K","Yang X","Chen Y","Justo MAR"],"additional_accession":[]},"is_claimable":false,"name":"CSNK2A1-mediated MAX phosphorylation upregulates HMGB1 and IL-6 expression in cholangiocarcinoma progression.","description":"<h4>Background</h4>We established a novel diethylnitrosamine (DEN) -induced mouse model that reflected the progression of cholangiocarcinoma (CCA) from atypical cystic hyperplasia.<h4>Methods</h4>BALB/c mice were administered DEN by oral gavage. Cells isolated from livers were analyzed for expression of CSNK2A1, MAX and MAX-interacting proteins. Human CCA cell lines (MzChA-1, HuCCT1), normal human cholangiocyte (H69), human hepatic stellate cells (LX-2), macrophages (RAW 264.7), and primary hepatic cells were used for cellular and molecular biology assays.<h4>Results</h4>Expression of MAX, CSNK2A1, C-MYC, β-catenin, HMGB1, and IL-6 was upregulated in hepatic cells from CCA liver tissue. The half-life of MAX is higher in CCA cells, and this favors their proliferation. Overexpression of MAX ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jul","modification":"2026-06-24T03:14:21.759Z","creation":"2026-06-24T03:07:25.663Z"},"accession":"S-EPMC10289747","cross_references":{"pubmed":["37347224"],"doi":["10.1097/HC9.0000000000000144"]}}