ArticleThoracic cancer2021
Silencing LINC01116 suppresses the development of lung adenocarcinoma via the AKT signaling pathway.
Article in Thoracic cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- High linc01116 expression may contribute to a poor prognosis in various cancers based on systematic reviews and meta-analyses.BMC cancer · 2024Pooled it
- LINC01116, a hypoxia-lncRNA marker of pathological lymphangiogenesis and poor prognosis in lung adenocarcinoma.Molecular oncology · 2026Article
- LncRNANon-coding RNA research · 2025Article
- The regulatory role and therapeutic potential of long non-coding RNA in non-small cell lung cancer.Journal of Cancer · 2025Review
- Long Non-Coding RNA LINC01116 Promotes the Proliferation of Lung Adenocarcinoma by Targeting miR-9-5p/CCNE1 Axis.Journal of cellular and molecular medicine · 2024Article
- Review
- LINC01116-dependent upregulation of RNA polymerase I transcription drives oncogenic phenotypes in lung adenocarcinoma.Journal of translational medicine · 2024Article
- Article
- Linc01116 Silencing Inhibits the Proliferation and Invasion, Promotes Apoptosis of Chordoma CellsCurrent molecular medicine · 2024Article
- Long non‑coding RNAs as potential therapeutic targets in non‑small cell lung cancer (Review).International journal of molecular medicine · 2023Review
- LINC01116 affects patient survival differently and is dissimilarly expressed in ER+ and ER- breast cancer samples.Cancer reports (Hoboken, N.J.) · 2023Article
- Construction of an algorithm based on oncosis-related LncRNAs comprising the molecular subtypes and a risk assessment model in lung adenocarcinoma.Journal of clinical laboratory analysis · 2022Article
- A novel senescence-related lncRNA signature that predicts prognosis and the tumor microenvironment in patients with lung adenocarcinoma.Frontiers in genetics · 2022Article
- Identification of an autophagy-related 12-lncRNA signature and evaluation of NFYC-AS1 as a pro-cancer factor in lung adenocarcinoma.Frontiers in genetics · 2022Article
- Silencing LINC01116 suppresses the development of lung adenocarcinoma via the AKT signaling pathway.Thoracic cancer · 2021Article
- An Immune-Related Long Noncoding RNA Signature as a Prognostic Biomarker for Human Endometrial Cancer.Journal of oncology · 2021Article
- Promising Advances in LINC01116 Related to Cancer.Frontiers in cell and developmental biology · 2021Review
- Construction of a Novel Lung Adenocarcinoma Immune-Related lncRNA Pair Signature.International journal of general medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA growing body of evidence has proven that long noncoding ribonucleic acids (lncRNAs) are important epigenetic regulators that play crucial parts in the pathogenesis of human cancers. Previous studies have shown that long intergenic nonprotein coding RNA 01116 (LINC01116) is a carcinogen in several carcinomas; however, its function in lung adenocarcinoma (LUAD) has not been clarified. Here, we aimed to investigate the role of LINC01116 in LUAD.
methodsThe relative expression levels of LINC01116 in LUAD cell lines and tissues were detected by quantitative reverse transcription polymerase chain reaction. A Kaplan-Meier survival analysis was performed using patient information from the Gene Expression Profiling Interactive Analysis (GEPIA) database. LUAD proliferation, invasion, migration, and apoptosis were measured by performing cell counting kit-8, colony formation, transwell, wound healing, and flow cytometric assays. A xenograft animal experiment was performed to investigate the effect of LINC01116 in vivo. Protein kinase B (AKT) signaling pathway-related protein expressions were tested by Western blot assay.
resultsLINC01116 expression was upregulated in LUAD cells and tissues. The loss-of-function experiments on LUAD cells revealed that silencing LINC01116 expression could decrease cell viability both in vitro and in vivo. Furthermore, silencing LINC01116 inhibited LUAD cell invasion and migration and induced cell apoptosis. Mechanically, silencing LINC01116 significantly decreased p-AKT protein levels, and an AKT pathway stimulator could rescue the suppressive effects of small interfering LINC011116-specific RNAs on LUAD development.
conclusionsOur study demonstrated that silencing LINC01116 suppresses the development of LUAD via the AKT signaling pathway.
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