<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>43(1)</volume><submitter>Li G</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>N4-Acetylcytidine (ac4C), a highly conserved post-transcriptional mechanism, plays a pivotal role in RNA modification and tumor progression. However, the molecular mechanism by which ac4C modification mediates tumor immunosuppression remains elusive in triple-negative breast cancer (TNBC).&lt;h4>Methods&lt;/h4>NAT10 expression was analyzed in TNBC samples in the level of mRNA and protein, and compared with the corresponding normal tissues. ac4C modification levels also measured in the TNBC samples. The effects of NAT10 on immune microenvironment and tumor metabolism were investigated. NAT10-mediated ac4C and its downstream regulatory mechanisms were determined in vitro and in vivo. The combination therapy of targeting NAT10 in TNBC was further explored.&lt;h4>Results&lt;/h4>The resu</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pagination>278</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11451012</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>NAT10/ac4C/JunB facilitates TNBC malignant progression and immunosuppression by driving glycolysis addiction.</pubmed_title><pmcid>PMC11451012</pmcid><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Liu L</pubmed_authors><pubmed_authors>Ma X</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Hao Y</pubmed_authors><pubmed_authors>Sui S</pubmed_authors><pubmed_authors>Yang Z</pubmed_authors><pubmed_authors>Wang Q</pubmed_authors><pubmed_authors>Tao W</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>He X</pubmed_authors><pubmed_authors>Xu S</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Yang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>NAT10/ac4C/JunB facilitates TNBC malignant progression and immunosuppression by driving glycolysis addiction.</name><description>&lt;h4>Background&lt;/h4>N4-Acetylcytidine (ac4C), a highly conserved post-transcriptional mechanism, plays a pivotal role in RNA modification and tumor progression. However, the molecular mechanism by which ac4C modification mediates tumor immunosuppression remains elusive in triple-negative breast cancer (TNBC).&lt;h4>Methods&lt;/h4>NAT10 expression was analyzed in TNBC samples in the level of mRNA and protein, and compared with the corresponding normal tissues. ac4C modification levels also measured in the TNBC samples. The effects of NAT10 on immune microenvironment and tumor metabolism were investigated. NAT10-mediated ac4C and its downstream regulatory mechanisms were determined in vitro and in vivo. The combination therapy of targeting NAT10 in TNBC was further explored.&lt;h4>Results&lt;/h4>The resu</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2025-04-18T15:55:52.648Z</modification><creation>2025-04-07T02:50:14.112Z</creation></dates><accession>S-EPMC11451012</accession><cross_references><pubmed>39363363</pubmed><doi>10.1186/s13046-024-03200-x</doi></cross_references></HashMap>