<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang Y</submitter><funding>Science &amp;amp; Technology Program of Guangzhou City</funding><funding>Program of Department of Natural Resources of Guangdong Province</funding><funding>Science &amp; Technology Program of Guangzhou City</funding><funding>Special Funds for the Cultivation of Guangdong College Students&amp;apos; Scientific and Technological Innovation</funding><funding>Special Funds for the Cultivation of Guangdong College Students' Scientific and Technological Innovation</funding><funding>Guangdong Basic and Applied Basic Research Foundation</funding><funding>National Natural Science Foundation of China</funding><funding>Guangdong Provincial Key R&amp;amp;D Programme</funding><funding>Guangdong Provincial Key R&amp;D Programme</funding><pagination>96</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10122280</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide, but current treatment options remain limited and cause serious life-threatening side effects. Aberrant FGFR4 signaling has been validated as an oncogenic driver of HCC, and EZH2, the catalytic subunit of the PRC2 complex, is a potential factor that contributes to acquired drug resistance in many tumors, including HCC. However, the functional relationship between these two carcinogenic factors, especially their significance for HCC treatment, remains unclear. In this study, we systematically evaluated the feasibility of a combination therapy targeting FGFR4 and EZH2 for HCC.&lt;h4>Methods&lt;/h4>RNA sequencing data of patients with Liver hepatocellular carcinoma (LIHC) from The Cancer Genome </pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>FGFR4 and EZH2 inhibitors synergistically induce hepatocellular carcinoma apoptosis via repressing YAP signaling.</pubmed_title><pmcid>PMC10122280</pmcid><funding_grant_id>2022A1515110620</funding_grant_id><funding_grant_id>GDNRC [2021] 50</funding_grant_id><funding_grant_id>20212210007</funding_grant_id><funding_grant_id>81902801</funding_grant_id><funding_grant_id>pdjh2021a0051</funding_grant_id><funding_grant_id>2022B1111070007</funding_grant_id><funding_grant_id>82273833</funding_grant_id><funding_grant_id>82173729</funding_grant_id><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Cao J</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Liu R</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Hong A</pubmed_authors><pubmed_authors>Zhang P</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Xie J</pubmed_authors><pubmed_authors>Su Z</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors></additional><is_claimable>false</is_claimable><name>FGFR4 and EZH2 inhibitors synergistically induce hepatocellular carcinoma apoptosis via repressing YAP signaling.</name><description>&lt;h4>Background&lt;/h4>Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide, but current treatment options remain limited and cause serious life-threatening side effects. Aberrant FGFR4 signaling has been validated as an oncogenic driver of HCC, and EZH2, the catalytic subunit of the PRC2 complex, is a potential factor that contributes to acquired drug resistance in many tumors, including HCC. However, the functional relationship between these two carcinogenic factors, especially their significance for HCC treatment, remains unclear. In this study, we systematically evaluated the feasibility of a combination therapy targeting FGFR4 and EZH2 for HCC.&lt;h4>Methods&lt;/h4>RNA sequencing data of patients with Liver hepatocellular carcinoma (LIHC) from The Cancer Genome </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2026-07-15T01:27:47.577Z</modification><creation>2026-06-27T03:14:29.093Z</creation></dates><accession>S-EPMC10122280</accession><cross_references><pubmed>37085881</pubmed><doi>10.1186/s13046-023-02659-4</doi></cross_references></HashMap>