ArticleCell death & disease2025
SP-1-activated LINC01016 overexpression promotes gastric cancer invasion and metastasis through inhibiting EIF4A3-mediated MMP9 mRNA decay.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- LncRNA LINC01579/miR-579-3p axis promotes gastric cancer progression via NOTCH1 pathway.World journal of surgical oncology · 2026Article
- LncRNA nonnmmut065573 promotes post-myocardial infarction cardiac fibrosis and activates the TGF-β1/ZEB1 pathway.Cell regeneration (London, England) · 2026Article
- FBXW7 suppresses gastric cancer development and progression via ubiquitination-mediated degradation of MMP2.Frontiers in immunology · 2026Article
- Identification of an m7G-Related lncRNA Signature for Prognostic Prediction and Immune Landscape Characterization in Early Gastric Cancer.OncoTargets and therapy · 2026Article
- Long Non-Coding TP73-AS1: A Potential Biomarker and Therapeutic Target in Cancer.International journal of molecular sciences · 2025Review
- Development of a PANoptosis-related LncRNAs for prognosis predicting and immune infiltration characterization of gastric Cancer.Scientific reports · 2025Article
- Silibinin-derived microbiota enrich (R)-2,3-dihydroxy-isovalerate and ameliorate colitis via the GAT-3/RARβ/RORγt axis.The ISME journal · 2025Article
- Case Report: Acute kidney injury due to minimal dilated obstructive nephropathy in the context of gastric cancer.Frontiers in oncology · 2025Article
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4 authors.
Funding
Abstract
Long noncoding RNAs (lncRNAs) are key regulators during gastric cancer (GC) development and may be viable treatment targets. In the present study, we showed that the expression of the long intergenic noncoding RNA 01016 (LINC01016) is significantly higher in GC tissues with lymph node metastasis (LNM) than those without LNM. LINC01016 overexpression predicts a poorer relapse-free survival (RFS) and overall survival (OS). Furthermore, we found that LINC01016 is activated by transcriptional factor SP-1 and contributes to the overt promotion of cell migratory ability. EIF4A3 was identified as a binding partner of LINC01016 by RNA pull-down assay, mass spectrometry and western blot. We determined that LINC01016 can blocks the binding of EIF4A3 to MMP9 mRNA, thereby inhibiting EIF4A3-mediated nonsense-mediated RNA decay (NMD), increasing MMP9 mRNA level and protein expression levels to promote tumor progression. LINC01016 or LINC01016-mediated EIF4A3/MMP9 may be potential therapeutic targets for patients with GC.
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