<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu Z</submitter><funding>Shanghai Science and Technology Committee</funding><funding>Science and Technology Commission of Shanghai Municipality</funding><funding>National Natural Science Foundation of China</funding><pagination>e2407517</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11633487</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(46)</volume><pubmed_abstract>Tumor immune microenvironment is strongly associated with the malignancy behavior of hepatocellular carcinoma (HCC). However, the immune function and regulatory mechanisms of B cells in HCC remain unclear. The expression differences between B cell high- and low-infiltration HCC samples are explored to identify the key regulator. Pre-mRNA processing factor 19 (PRP19) expression is increased in B cell low-infiltrated tissues and negatively correlated with the B cell marker, CD20. Inhibition of PRP19 expression promoted B cell infiltration in tumor tissue and impeded HCC growth. Mechanically, the co-immunoprecipitation (Co-IP) assay revealed that PRP19 interacts with DEAD-box helicase 5 (DDX5), leading to ubiquitination and degradation of the DDX5 protein. The attenuated DDX5 impairs CXCL12 m</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>Increased PRP19 in Hepatocyte Impedes B Cell Function to Promote Hepatocarcinogenesis.</pubmed_title><pmcid>PMC11633487</pmcid><funding_grant_id>82203863</funding_grant_id><funding_grant_id>20Y11908100</funding_grant_id><funding_grant_id>82403314</funding_grant_id><funding_grant_id>82173122</funding_grant_id><funding_grant_id>82273027</funding_grant_id><funding_grant_id>81972234</funding_grant_id><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Zhang D</pubmed_authors><pubmed_authors>Xue R</pubmed_authors><pubmed_authors>Lin X</pubmed_authors><pubmed_authors>Dong L</pubmed_authors><pubmed_authors>Guo D</pubmed_authors><pubmed_authors>Tang W</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Shen X</pubmed_authors><pubmed_authors>Yu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Increased PRP19 in Hepatocyte Impedes B Cell Function to Promote Hepatocarcinogenesis.</name><description>Tumor immune microenvironment is strongly associated with the malignancy behavior of hepatocellular carcinoma (HCC). However, the immune function and regulatory mechanisms of B cells in HCC remain unclear. The expression differences between B cell high- and low-infiltration HCC samples are explored to identify the key regulator. Pre-mRNA processing factor 19 (PRP19) expression is increased in B cell low-infiltrated tissues and negatively correlated with the B cell marker, CD20. Inhibition of PRP19 expression promoted B cell infiltration in tumor tissue and impeded HCC growth. Mechanically, the co-immunoprecipitation (Co-IP) assay revealed that PRP19 interacts with DEAD-box helicase 5 (DDX5), leading to ubiquitination and degradation of the DDX5 protein. The attenuated DDX5 impairs CXCL12 m</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-02T11:17:45.929Z</modification><creation>2025-04-06T15:06:52.832Z</creation></dates><accession>S-EPMC11633487</accession><cross_references><pubmed>39422063</pubmed><doi>10.1002/advs.202407517</doi></cross_references></HashMap>