<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liang B</submitter><funding>NIDDK NIH HHS</funding><funding>Burroughs Wellcome Fund</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><pagination>120-131</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8217095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>75(1)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Gain of function (GOF) mutations in the CTNNB1 gene are one of the most frequent genetic events in hepatocellular carcinoma (HCC). T-box transcription factor 3 (TBX3) is a liver-specific target of the Wnt/β-catenin pathway and thought to be an oncogene mediating activated β-catenin-driven HCC formation.&lt;h4>Methods&lt;/h4>We evaluated the expression pattern of TBX3 in human HCC specimens. Tbx3 was conditionally knocked out in murine HCC models by hydrodynamic tail vein injection of Cre together with c-Met and ΔN90-β-catenin (c-Met/β-catenin) in Tbx3&lt;sup>flox/flox&lt;/sup> mice. TBX3 was overexpressed in human HCC cell lines to investigate the functions of TBX3 in vitro.&lt;h4>Results&lt;/h4>A bimodal expression pattern of TBX3 in human HCC samples was detected: high expression</pubmed_abstract><journal>Journal of hepatology</journal><pubmed_title>TBX3 functions as a tumor suppressor downstream of activated CTNNB1 mutants during hepatocarcinogenesis.</pubmed_title><pmcid>PMC8217095</pmcid><funding_grant_id>P30 DK026743</funding_grant_id><funding_grant_id>P30 DK120531</funding_grant_id><funding_grant_id>P30DK026743</funding_grant_id><funding_grant_id>R01 CA251155</funding_grant_id><funding_grant_id>R01 CA239251</funding_grant_id><funding_grant_id>R01CA239251</funding_grant_id><funding_grant_id>R01 CA250227</funding_grant_id><funding_grant_id>K08DK101603</funding_grant_id><funding_grant_id>R01CA204586</funding_grant_id><funding_grant_id>R01CA250227</funding_grant_id><funding_grant_id>K08 DK101603</funding_grant_id><funding_grant_id>R01 CA204586</funding_grant_id><pubmed_authors>Xu M</pubmed_authors><pubmed_authors>Lin S</pubmed_authors><pubmed_authors>Wang B</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Zhou Y</pubmed_authors><pubmed_authors>Monga SP</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Ren C</pubmed_authors><pubmed_authors>Evert M</pubmed_authors><pubmed_authors>Liang B</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Song X</pubmed_authors><pubmed_authors>Calvisi DF</pubmed_authors><pubmed_authors>Qian M</pubmed_authors></additional><is_claimable>false</is_claimable><name>TBX3 functions as a tumor suppressor downstream of activated CTNNB1 mutants during hepatocarcinogenesis.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Gain of function (GOF) mutations in the CTNNB1 gene are one of the most frequent genetic events in hepatocellular carcinoma (HCC). T-box transcription factor 3 (TBX3) is a liver-specific target of the Wnt/β-catenin pathway and thought to be an oncogene mediating activated β-catenin-driven HCC formation.&lt;h4>Methods&lt;/h4>We evaluated the expression pattern of TBX3 in human HCC specimens. Tbx3 was conditionally knocked out in murine HCC models by hydrodynamic tail vein injection of Cre together with c-Met and ΔN90-β-catenin (c-Met/β-catenin) in Tbx3&lt;sup>flox/flox&lt;/sup> mice. TBX3 was overexpressed in human HCC cell lines to investigate the functions of TBX3 in vitro.&lt;h4>Results&lt;/h4>A bimodal expression pattern of TBX3 in human HCC samples was detected: high expression</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jul</publication><modification>2026-05-08T01:13:07.428Z</modification><creation>2022-07-10T09:34:20.069Z</creation></dates><accession>S-EPMC8217095</accession><cross_references><pubmed>33577921</pubmed><doi>10.1016/j.jhep.2021.01.044</doi></cross_references></HashMap>