<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>26(1)</volume><submitter>Luo Y</submitter><pubmed_abstract>Our study aims to investigate the roles of embryonic lethal abnormal vision-like 1 (ELAVL1) and long non-coding RNA (LncRNA) NEAT1 in endometrial cancer (EC), focusing on their underlying molecular mechanisms.We obtained EC cell lines (HEC-1A, Ishikawa, RL95-2, HEC-1B, and AN3CA) from ATCC. We used siRNAs (si-ELAVL1#1 and si-ELAVL1#2) and overexpression RNAs (OE ELAVL1 and OE-NEAT1) for knockdown or overexpression of ELAVL1 and LncRNA NEAT1. We also employed 3-MA (5mM) or rapamycin (100µM) to inhibit or promote autophagy. Moreover, we conducted RNA immunoprecipitation (RIP) assays to confirm the interaction between LncRNA NEAT1 and ELAVL1. Cell Counting Kit-8 (CCK-8) and transwell assays were utilized to assess cell proliferation and migration. Additionally, we measured the expression of E</pubmed_abstract><journal>Cancer biology &amp; therapy</journal><pagination>2469927</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11875488</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability.</pubmed_title><pmcid>PMC11875488</pmcid><pubmed_authors>Fan J</pubmed_authors><pubmed_authors>Luo Y</pubmed_authors><pubmed_authors>Zhong X</pubmed_authors><pubmed_authors>Sun X</pubmed_authors></additional><is_claimable>false</is_claimable><name>The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability.</name><description>Our study aims to investigate the roles of embryonic lethal abnormal vision-like 1 (ELAVL1) and long non-coding RNA (LncRNA) NEAT1 in endometrial cancer (EC), focusing on their underlying molecular mechanisms.We obtained EC cell lines (HEC-1A, Ishikawa, RL95-2, HEC-1B, and AN3CA) from ATCC. We used siRNAs (si-ELAVL1#1 and si-ELAVL1#2) and overexpression RNAs (OE ELAVL1 and OE-NEAT1) for knockdown or overexpression of ELAVL1 and LncRNA NEAT1. We also employed 3-MA (5mM) or rapamycin (100µM) to inhibit or promote autophagy. Moreover, we conducted RNA immunoprecipitation (RIP) assays to confirm the interaction between LncRNA NEAT1 and ELAVL1. Cell Counting Kit-8 (CCK-8) and transwell assays were utilized to assess cell proliferation and migration. Additionally, we measured the expression of E</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2025-04-04T01:12:37.007Z</modification><creation>2025-04-04T01:12:37.007Z</creation></dates><accession>S-EPMC11875488</accession><cross_references><pubmed>40018990</pubmed><doi>10.1080/15384047.2025.2469927</doi></cross_references></HashMap>