<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Shen M</submitter><funding>Wuxi City Health Commission Maternal and Child Health Scientific Research Project Plan</funding><pagination>31502</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11682247</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in cancer progression. We found lncRNA DNM1P35 is elevated in ovarian tumors compared to normal tissues, and demonstrated that lncRNA DNM1P35 promoted cancer cell proliferation, migration and invasion in SK-OV-3 and OVCAR-3 cell lines. Furthermore, lncRNA DNM1P35 also facilitated the epithelial-mesenchymal transition (EMT) of ovarian cancer cells. Mechanistic studies identified microRNA-326 (miR-326) as a target of lncRNA DNM1P35. Overexpression of miR-326 diminished the tumor-promoting activity of lncRNA DNM1P35, resulting in reduction of Zinc finger E-box-binding homeobox 1 (ZEB1) expression and EMT features. We further revealed that ZEB1, a master transcription factor for EMT that is negatively regulated by miR-326, was e</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>LncRNA DNM1P35 sponges hsa-mir-326 to promote ovarian cancer progression.</pubmed_title><pmcid>PMC11682247</pmcid><funding_grant_id>FYKY202301</funding_grant_id><pubmed_authors>Shen M</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Mao Y</pubmed_authors><pubmed_authors>Zhang Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>LncRNA DNM1P35 sponges hsa-mir-326 to promote ovarian cancer progression.</name><description>Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in cancer progression. We found lncRNA DNM1P35 is elevated in ovarian tumors compared to normal tissues, and demonstrated that lncRNA DNM1P35 promoted cancer cell proliferation, migration and invasion in SK-OV-3 and OVCAR-3 cell lines. Furthermore, lncRNA DNM1P35 also facilitated the epithelial-mesenchymal transition (EMT) of ovarian cancer cells. Mechanistic studies identified microRNA-326 (miR-326) as a target of lncRNA DNM1P35. Overexpression of miR-326 diminished the tumor-promoting activity of lncRNA DNM1P35, resulting in reduction of Zinc finger E-box-binding homeobox 1 (ZEB1) expression and EMT features. We further revealed that ZEB1, a master transcription factor for EMT that is negatively regulated by miR-326, was e</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2026-06-01T21:58:51.281Z</modification><creation>2025-04-04T21:49:23.615Z</creation></dates><accession>S-EPMC11682247</accession><cross_references><pubmed>39732940</pubmed><doi>10.1038/s41598-024-83170-4</doi></cross_references></HashMap>