ArticleAging2024
LncRNA HAGLR regulates gastric cancer progression by regulating the miR-20a-5p/E2F1 axis.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- ESPNP promotes cell migration and invasion in gastric cancer cells via regulation of epithelial-mesenchymal transition/Twist1.Journal of molecular histology · 2026Article
- Biomarker-Based Precision Prediction of Immunotherapy Response in Hepatocellular Carcinoma.Diagnostics (Basel, Switzerland) · 2025Article
- Mitochondrial autophagy-related lncRNAs as prognostic biomarkers and therapeutic targets in gastric adenocarcinoma.Discover oncology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric 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.
methodsThe 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
resultsElevated 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.
conclusionsThe data suggest that the HAGLR/miR-20a-5p/E2F1 regulatory cascade is implicated in GC pathogenesis, offering a novel therapeutic avenue for GC management.
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