<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Pu J</submitter><funding>Guangxi Science and Technology plan Project</funding><funding>Guangxi Natural Science Foundation Project</funding><pagination>3649-3665</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10475779</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>114(9)</volume><pubmed_abstract>As an epitranscriptomic modulation manner, N&lt;sup>6&lt;/sup> -methyladenosine (m&lt;sup>6&lt;/sup> A) modification plays important roles in various diseases, including hepatocellular carcinoma (HCC). m&lt;sup>6&lt;/sup> A modification affects the fate of RNAs. The potential contributions of m&lt;sup>6&lt;/sup> A to the functions of RNA still need further investigation. In this study, we identified long noncoding RNA FAM111A-DT as an m&lt;sup>6&lt;/sup> A-modified RNA and confirmed three m&lt;sup>6&lt;/sup> A sites on FAM111A-DT. The m&lt;sup>6&lt;/sup> A modification level of FAM111A-DT was increased in HCC tissues and cell lines, and increased m&lt;sup>6&lt;/sup> A level was correlated with poor survival of HCC patients. m&lt;sup>6&lt;/sup> A modification increased the stability of FAM111A-DT transcript, whose expression level showed simil</pubmed_abstract><journal>Cancer science</journal><pubmed_title>N&lt;sup>6&lt;/sup> -methyladenosine-modified FAM111A-DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A.</pubmed_title><pmcid>PMC10475779</pmcid><funding_grant_id>2021AC20006</funding_grant_id><funding_grant_id>2019GXNSFBA245023</funding_grant_id><funding_grant_id>2020GXNSFAA259019</funding_grant_id><pubmed_authors>Huang Y</pubmed_authors><pubmed_authors>Wei Q</pubmed_authors><pubmed_authors>Huang Z</pubmed_authors><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Fang Q</pubmed_authors><pubmed_authors>Pu J</pubmed_authors><pubmed_authors>Wei H</pubmed_authors><pubmed_authors>Nian J</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Xu Z</pubmed_authors><pubmed_authors>Liu G</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>N&lt;sup>6&lt;/sup> -methyladenosine-modified FAM111A-DT promotes hepatocellular carcinoma growth via epigenetically activating FAM111A.</name><description>As an epitranscriptomic modulation manner, N&lt;sup>6&lt;/sup> -methyladenosine (m&lt;sup>6&lt;/sup> A) modification plays important roles in various diseases, including hepatocellular carcinoma (HCC). m&lt;sup>6&lt;/sup> A modification affects the fate of RNAs. The potential contributions of m&lt;sup>6&lt;/sup> A to the functions of RNA still need further investigation. In this study, we identified long noncoding RNA FAM111A-DT as an m&lt;sup>6&lt;/sup> A-modified RNA and confirmed three m&lt;sup>6&lt;/sup> A sites on FAM111A-DT. The m&lt;sup>6&lt;/sup> A modification level of FAM111A-DT was increased in HCC tissues and cell lines, and increased m&lt;sup>6&lt;/sup> A level was correlated with poor survival of HCC patients. m&lt;sup>6&lt;/sup> A modification increased the stability of FAM111A-DT transcript, whose expression level showed simil</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Sep</publication><modification>2026-05-28T18:05:22.332Z</modification><creation>2025-04-07T04:14:12.772Z</creation></dates><accession>S-EPMC10475779</accession><cross_references><pubmed>37400994</pubmed><doi>10.1111/cas.15886</doi></cross_references></HashMap>