Research Paper|Volume 16, Issue 16|pp 11843—11856

LncRNA HAGLR regulates gastric cancer progression by regulating the miR-20a-5p/E2F1 axis

Qingwei Liu¹, Yong Li¹, Bibo Tan¹, Qun Zhao¹, Liqiao Fan¹, Zhidong Zhang¹, Dong Wang¹, Xuefeng Zhao¹, Yu Liu¹, Wenbo Liu¹

¹The Third Department of Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China

Received: August 21, 2023Accepted: May 30, 2024Published: August 21, 2024

https://doi.org/10.18632/aging.206039

Copyright: © 2024 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Gastric cancer (GC) stands as a prevalent and challenging malignancy within the gastrointestinal tract. The potential of long non-coding RNAs (lncRNAs) as biomarkers and therapeutic targets in oncology has garnered immense research interest. This study aims to elucidate the relevance, biological roles, and mechanistic pathways of LncRNA HAGLR in the context of GC.

Methods: The assessments of cell proliferation, migration, and invasion were executed using CCK-8, wound healing, and Transwell assays. The interactions between HAGLR, miR-20a-5p, and E2F1 were appraised through luciferase reporter assays, fluorescence in situ hybridization (FISH), and RNA immunoprecipitation (RIP). A tumor xenograft model provided in vivo validation for in vitro findings.

Results: Elevated levels of HAGLR in GC cells and tissue specimens were linked to worse patient outcomes. The inhibition of HAGLR led to a decrease in GC cell proliferation, migration, and invasion, whereas its activation prompted contrary effects. The impact of HAGLR on cell migration and invasion was notably associated with epithelial-mesenchymal transition (EMT). Through bioinformatics, luciferase reporter assays, FISH, RIP, and Western blot analyses, it was revealed that HAGLR acts as a molecular sponge for miR-20a-5p, consequently augmenting E2F1 levels.

Conclusions: The data suggest that the HAGLR/miR-20a-5p/E2F1 regulatory cascade is implicated in GC pathogenesis, offering a novel therapeutic avenue for GC management.