The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability

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...

Full description

Saved in:
Bibliographic Details
Main Authors: Yanlu Luo, Xueyan Zhong, Xinzhao Sun, Jiangtao Fan
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Cancer Biology & Therapy
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/15384047.2025.2469927
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849716714125656064
author Yanlu Luo
Xueyan Zhong
Xinzhao Sun
Jiangtao Fan
author_facet Yanlu Luo
Xueyan Zhong
Xinzhao Sun
Jiangtao Fan
author_sort Yanlu Luo
collection DOAJ
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 ELAVL1 and Beclin1 through Western blotting and RT-qPCR.ELAVL1 was found to be highly expressed in EC. Furthermore, ELAVL1 promoted the proliferation, invasion, and migration of EC cells through the regulation of Beclin1-related pathways. RIP assays revealed a direct interaction between LncRNA NEAT1 and ELAVL1, with ELAVL1 stabilizing LncRNA NEAT1 mRNA in EC cells. Additionally, we observed that ELAVL1 influenced EC cell proliferation, invasion, and migration through the regulation of LncRNA NEAT1-mediated regulation of Beclin1 expression. Moreover, in an animal study, we determined that ELAVL1 influenced endometrial cancer tumor growth through its interaction with LncRNA NEAT1, which mediated Beclin1 expression in vivo.In summary, our study showed that ELAVL1 regulated the malignant behavior of endometrial cancer cells through the modulation of LncRNA NEAT1-mediated regulation of Beclin1 expression.
format Article
id doaj-art-ebe9544407e046318b8574f43ede2cdd
institution DOAJ
issn 1538-4047
1555-8576
language English
publishDate 2025-12-01
publisher Taylor & Francis Group
record_format Article
series Cancer Biology & Therapy
spelling doaj-art-ebe9544407e046318b8574f43ede2cdd2025-08-20T03:12:54ZengTaylor & Francis GroupCancer Biology & Therapy1538-40471555-85762025-12-0126110.1080/15384047.2025.2469927The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stabilityYanlu Luo0Xueyan Zhong1Xinzhao Sun2Jiangtao Fan3Department of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. ChinaDepartment of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. ChinaDepartment of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. ChinaDepartment of Gynecology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. ChinaOur 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 ELAVL1 and Beclin1 through Western blotting and RT-qPCR.ELAVL1 was found to be highly expressed in EC. Furthermore, ELAVL1 promoted the proliferation, invasion, and migration of EC cells through the regulation of Beclin1-related pathways. RIP assays revealed a direct interaction between LncRNA NEAT1 and ELAVL1, with ELAVL1 stabilizing LncRNA NEAT1 mRNA in EC cells. Additionally, we observed that ELAVL1 influenced EC cell proliferation, invasion, and migration through the regulation of LncRNA NEAT1-mediated regulation of Beclin1 expression. Moreover, in an animal study, we determined that ELAVL1 influenced endometrial cancer tumor growth through its interaction with LncRNA NEAT1, which mediated Beclin1 expression in vivo.In summary, our study showed that ELAVL1 regulated the malignant behavior of endometrial cancer cells through the modulation of LncRNA NEAT1-mediated regulation of Beclin1 expression.https://www.tandfonline.com/doi/10.1080/15384047.2025.2469927ELAVL1endometrial cancerautophagyLncRNA-NEAT
spellingShingle Yanlu Luo
Xueyan Zhong
Xinzhao Sun
Jiangtao Fan
The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
Cancer Biology & Therapy
ELAVL1
endometrial cancer
autophagy
LncRNA-NEAT
title The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
title_full The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
title_fullStr The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
title_full_unstemmed The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
title_short The RNA-binding protein ELAVL1 promotes Beclin1-mediated cellular autophagy and thus endometrial cancer development by affecting LncRNA-neat stability
title_sort rna binding protein elavl1 promotes beclin1 mediated cellular autophagy and thus endometrial cancer development by affecting lncrna neat stability
topic ELAVL1
endometrial cancer
autophagy
LncRNA-NEAT
url https://www.tandfonline.com/doi/10.1080/15384047.2025.2469927
work_keys_str_mv AT yanluluo thernabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT xueyanzhong thernabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT xinzhaosun thernabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT jiangtaofan thernabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT yanluluo rnabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT xueyanzhong rnabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT xinzhaosun rnabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability
AT jiangtaofan rnabindingproteinelavl1promotesbeclin1mediatedcellularautophagyandthusendometrialcancerdevelopmentbyaffectinglncrnaneatstability