ArticleOpen medicine (Warsaw, Poland)2023
Overexpression of LINC00607 inhibits cell growth and aggressiveness by regulating the miR-1289/EFNA5 axis in non-small-cell lung cancer.
Article in Open medicine (Warsaw, Poland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Long non-coding RNA LINC00607 epigenetically regulates endothelial TSPAN18 to promote hypoxia-induced thromboinflammation.The Journal of biological chemistry · 2026Article
- EIF4A3-Mediated downregulation of circPTEN promotes hepatocellular carcinoma progression through the miR-1289/RBM38 Axis.Journal of molecular histology · 2025Article
- Non-coding RNAs and exosomal non-coding RNAs in lung cancer: insights into their functions.Frontiers in cell and developmental biology · 2024Review
- Screening of Immune-related lncRNAs in Lung Adenocarcinoma and Establishing a Survival Prognostic Risk Prediction Model.Combinatorial chemistry & high throughput screening · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) play a key role in cancer progression, including non-small-cell lung cancer (NSCLC). LncRNA long intergenic non-protein-coding RNA 00607 (LINC00607) was previously discovered to be downregulated in lung adenocarcinoma tissues. Nevertheless, the potential role of LINC00607 in NSCLC is still unclear. The expression of LINC00607, miR-1289, and ephrin A5 (EFNA5) in NSCLC tissues and cells was tested by reverse transcription quantitative polymerase chain reaction. Cell viability, proliferation, migration, and invasion were measured by 3-(4,5-dimethylthiazole-2-y1)-2,5-diphenyl tetrazolium bromide, colony formation, wound healing, and Transwell assays. The relationship among LINC00607, miR-1289, and EFNA5 in NSCLC cells was verified by the luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation assay. In this study, LINC00607 was downregulated in NSCLC, and its low level is associated with poor prognosis of NSCLC patients. Furthermore, LINC00607 overexpression repressed NSCLC cell viability, proliferation, migration, and invasion. LINC00607 bound with miR-1289 in NSCLC. EFNA5 was a downstream target of miR-1289. EFNA5 overexpression also inhibited NSCLC cell viability, proliferation, migration, and invasion. EFNA5 knockdown antagonized the influence of LINC00607 overexpression on NSCLC cell phenotypes. Overall, LINC00607 serves as a tumor suppressor gene in NSCLC through binding with miR-1289 and modulating the level of EFNA5.
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