<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(11)</volume><submitter>Yuan Y</submitter><pubmed_abstract>Long non-coding RNAs (lncRNAs) have emerged as key regulators of cancer progression through their interaction with microRNAs and modulation of gene expression. However, their role in mitochondrial metabolism, particularly in non-small cell lung cancer (NSCLC), remains poorly defined. In this study, we found that LINC02802 was significantly upregulated in NSCLC tissues and associated with poor prognosis. Mechanistically, LINC02802 acts as a competing endogenous RNA (ceRNA) for miR-1976, thereby relieving the suppression of solute carrier family 25 member 51(SLC25A51). Elevated SLC25A51 enhances mitochondrial NAD&lt;sup>+&lt;/sup> import, leading to an increased NAD&lt;sup>+&lt;/sup>/NADH ratio and promoting oxidative TCA cycle flux. Functionally, this shift supports tumor cell proliferation and migrati</pubmed_abstract><journal>International journal of biological sciences</journal><pagination>4908-4926</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12374817</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>N4-acetylcytidine modification of LINC02802 promotes non-small cell lung cancer progression by modulating mitochondrial NAD+/NADH ratio.</pubmed_title><pmcid>PMC12374817</pmcid><pubmed_authors>Duan L</pubmed_authors><pubmed_authors>Zhang D</pubmed_authors><pubmed_authors>Tang L</pubmed_authors><pubmed_authors>Jiang X</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Yuan Y</pubmed_authors><pubmed_authors>Duan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>N4-acetylcytidine modification of LINC02802 promotes non-small cell lung cancer progression by modulating mitochondrial NAD+/NADH ratio.</name><description>Long non-coding RNAs (lncRNAs) have emerged as key regulators of cancer progression through their interaction with microRNAs and modulation of gene expression. However, their role in mitochondrial metabolism, particularly in non-small cell lung cancer (NSCLC), remains poorly defined. In this study, we found that LINC02802 was significantly upregulated in NSCLC tissues and associated with poor prognosis. Mechanistically, LINC02802 acts as a competing endogenous RNA (ceRNA) for miR-1976, thereby relieving the suppression of solute carrier family 25 member 51(SLC25A51). Elevated SLC25A51 enhances mitochondrial NAD&lt;sup>+&lt;/sup> import, leading to an increased NAD&lt;sup>+&lt;/sup>/NADH ratio and promoting oxidative TCA cycle flux. Functionally, this shift supports tumor cell proliferation and migrati</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-07-15T09:48:19.477Z</modification><creation>2026-07-02T03:11:52.776Z</creation></dates><accession>S-EPMC12374817</accession><cross_references><pubmed>40860186</pubmed><doi>10.7150/ijbs.116639</doi></cross_references></HashMap>