<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang B</submitter><funding>NIDDK NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>e00144</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10289747</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>We established a novel diethylnitrosamine (DEN) -induced mouse model that reflected the progression of cholangiocarcinoma (CCA) from atypical cystic hyperplasia.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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 </pubmed_abstract><journal>Hepatology communications</journal><pubmed_title>CSNK2A1-mediated MAX phosphorylation upregulates HMGB1 and IL-6 expression in cholangiocarcinoma progression.</pubmed_title><pmcid>PMC10289747</pmcid><funding_grant_id>R01 DK123763</funding_grant_id><funding_grant_id>R01 CA172086</funding_grant_id><funding_grant_id>R01 DK107288</funding_grant_id><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Fan W</pubmed_authors><pubmed_authors>Lu SC</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Barbier-Torres L</pubmed_authors><pubmed_authors>Yang B</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Steggerda J</pubmed_authors><pubmed_authors>Ramani K</pubmed_authors><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Justo MAR</pubmed_authors></additional><is_claimable>false</is_claimable><name>CSNK2A1-mediated MAX phosphorylation upregulates HMGB1 and IL-6 expression in cholangiocarcinoma progression.</name><description>&lt;h4>Background&lt;/h4>We established a novel diethylnitrosamine (DEN) -induced mouse model that reflected the progression of cholangiocarcinoma (CCA) from atypical cystic hyperplasia.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/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 </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jul</publication><modification>2026-06-24T03:14:21.759Z</modification><creation>2026-06-24T03:07:25.663Z</creation></dates><accession>S-EPMC10289747</accession><cross_references><pubmed>37347224</pubmed><doi>10.1097/HC9.0000000000000144</doi></cross_references></HashMap>