<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yuan XQ</submitter><funding>Fundamental Research Funds for the Central Universities</funding><funding>Basic and Applied Basic Research Foundation of Guangdong Province</funding><funding>Guangdong Provincial Natural Science Foundation</funding><funding>National Natural Science Foundation of China</funding><funding>China Postdoctoral Science Foundation</funding><funding>National Postdoctoral Program for Innovative Talents</funding><pagination>1756-1774</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10277835</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(6)</volume><pubmed_abstract>Super-enhancer (SE) plays a vital role in the determination of cell identity and fate. Up-regulated expression of coding genes is frequently associated with SE. However, the transcription dysregulation driven by SE, from the viewpoint of long non-coding RNA (lncRNA), remains unclear. Here, SE-associated lncRNAs in HCC are comprehensively outlined for the first time. This study integrally screens and identifies several novel SE-associated lncRNAs that are highly abundant and sensitive to JQ1. Especially, HSAL3 is identified as an uncharacterized SE-driven oncogenic lncRNA, which is activated by transcription factors HCFC1 and HSF1 via its super-enhancer. HSAL3 interference negatively regulates NOTCH signaling, implying the potential mechanism of its tumor-promoting role. The expression of H</pubmed_abstract><journal>Molecular therapy : the journal of the American Society of Gene Therapy</journal><pubmed_title>Anchoring super-enhancer-driven oncogenic lncRNAs for anti-tumor therapy in hepatocellular carcinoma.</pubmed_title><pmcid>PMC10277835</pmcid><funding_grant_id>2019A1515012114</funding_grant_id><funding_grant_id>81802812</funding_grant_id><funding_grant_id>2019M663254</funding_grant_id><funding_grant_id>2018A030313129</funding_grant_id><funding_grant_id>BX20190395</funding_grant_id><funding_grant_id>81803636</funding_grant_id><funding_grant_id>81972658</funding_grant_id><funding_grant_id>2018A0303130329</funding_grant_id><funding_grant_id>20ykpy105</funding_grant_id><pubmed_authors>Li GC</pubmed_authors><pubmed_authors>Wang JP</pubmed_authors><pubmed_authors>Zhou N</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Yuan XQ</pubmed_authors><pubmed_authors>Peng L</pubmed_authors><pubmed_authors>Yang XZ</pubmed_authors><pubmed_authors>Zhang CY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Anchoring super-enhancer-driven oncogenic lncRNAs for anti-tumor therapy in hepatocellular carcinoma.</name><description>Super-enhancer (SE) plays a vital role in the determination of cell identity and fate. Up-regulated expression of coding genes is frequently associated with SE. However, the transcription dysregulation driven by SE, from the viewpoint of long non-coding RNA (lncRNA), remains unclear. Here, SE-associated lncRNAs in HCC are comprehensively outlined for the first time. This study integrally screens and identifies several novel SE-associated lncRNAs that are highly abundant and sensitive to JQ1. Especially, HSAL3 is identified as an uncharacterized SE-driven oncogenic lncRNA, which is activated by transcription factors HCFC1 and HSF1 via its super-enhancer. HSAL3 interference negatively regulates NOTCH signaling, implying the potential mechanism of its tumor-promoting role. The expression of H</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2026-06-01T10:59:10.924Z</modification><creation>2026-04-08T11:40:23.232Z</creation></dates><accession>S-EPMC10277835</accession><cross_references><pubmed>36461633</pubmed><doi>10.1016/j.ymthe.2022.11.013</doi></cross_references></HashMap>