<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu W</submitter><funding>Liaoning Province talent plan project</funding><funding>Innovative Teams Project in Key Areas of Dalian</funding><funding>Dalian Medical Science Research Program</funding><pagination>256</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12433413</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>151(9)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>The study aimed to investigate the role of FBXW11 in hepatocellular carcinoma (HCC) and its underlying mechanism. Specifically, we explored whether FBXW11 inhibits tumorigenesis by regulating YB1 ubiquitination and elucidated the functional significance of the FBXW11-YB1 axis in HCC progression.&lt;h4>Methods&lt;/h4>Clinical HCC specimens and cell lines (HCC-LM3, HuH7, Hep3B, SNU-449) were used. FBXW11 and YB1 expression were analyzed via Western blotting and immunohistochemistry (IHC). Gain- and loss-of-function assays (FBXW11 overexpression/knockdown) were performed to assess cell proliferation. Co-immunoprecipitation (Co-IP), mass spectrometry, and ubiquitination assays identified protein interactions and ubiquitination patterns. In vivo tumorigenesis was evaluated using xenog</pubmed_abstract><journal>Journal of cancer research and clinical oncology</journal><pubmed_title>FBXW11 inhibits tumorigenesis by ubiquitinating YB1 in hepatocarcinoma.</pubmed_title><pmcid>PMC12433413</pmcid><funding_grant_id>2021RT01</funding_grant_id><funding_grant_id>YXMJ-JC-04</funding_grant_id><funding_grant_id>2312016</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Xu B</pubmed_authors><pubmed_authors>Wang T</pubmed_authors><pubmed_authors>Dong C</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>FBXW11 inhibits tumorigenesis by ubiquitinating YB1 in hepatocarcinoma.</name><description>&lt;h4>Purpose&lt;/h4>The study aimed to investigate the role of FBXW11 in hepatocellular carcinoma (HCC) and its underlying mechanism. Specifically, we explored whether FBXW11 inhibits tumorigenesis by regulating YB1 ubiquitination and elucidated the functional significance of the FBXW11-YB1 axis in HCC progression.&lt;h4>Methods&lt;/h4>Clinical HCC specimens and cell lines (HCC-LM3, HuH7, Hep3B, SNU-449) were used. FBXW11 and YB1 expression were analyzed via Western blotting and immunohistochemistry (IHC). Gain- and loss-of-function assays (FBXW11 overexpression/knockdown) were performed to assess cell proliferation. Co-immunoprecipitation (Co-IP), mass spectrometry, and ubiquitination assays identified protein interactions and ubiquitination patterns. In vivo tumorigenesis was evaluated using xenog</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-04-08T19:52:07.522Z</modification><creation>2026-04-08T14:35:43.283Z</creation></dates><accession>S-EPMC12433413</accession><cross_references><pubmed>40944757</pubmed><doi>10.1007/s00432-025-06307-6</doi></cross_references></HashMap>