ArticleDiscover oncology2025
miR-17-5p is highly expressed in patients with lung cancer and promoted lung cancer by targeting SIK1.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Targeting Spatiotemporal Heterogeneity of oncomiRNAs: A New Frontier in Cancer Therapy.Cancer reports (Hoboken, N.J.) · 2026Review
- MiracleNet: A Biologically Interpretable Machine Learning Model for Resected Non-small-cell Lung Cancer.Computational and structural biotechnology journal · 2026Article
- miR-17: from developmental regulatory hub to molecular engine driving tumourigenesis.Frontiers in oncology · 2026Review
- Upregulation of a MicroRNA Signature Involving miR-17-5p, miR-26b-5p, miR-106a-5p, and miR-146a-5p During Cervical Epithelial Transformation.Epigenomes · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to investigate the expression and role of miR-17-5p in lung cancer.
methodsThe levels of miR-17-5p in four non-small cell lung cancer cell lines and human normal lung epithelial cells (BEAS-2B) were detected by fluorescent quantitative PCR. Next, the cell lines with relatively high expression of miR-17-5p were treated with miR-17-5p mimics, miR-17-5p inhibitor or control miRNA. CCK8, flow cytometry analysis, and Transwell assay were used to analyze cell proliferation, apoptosis, invasion, and migration. The target genes of miR-17-5p were predicted based on Starbase and Targetscan databases, and the interaction between miR-17-5p and SIK1 was verified by luciferase assay.
resultsmiR-17-5p was highly expressed in lung cancer tissues of patients with lung cancer. Overexpression of miR-17-5p significantly promoted lung adenocarcinoma cell proliferation, invasion, and migration, and inhibited apoptosis. There was a direct binding site between miR-17-5p and SIK1 3'UTR, and overexpression of miR-17-5p inhibited the expression of SIK1 at both mRNA and protein levels.
conclusionOur findings suggest that miR-17-5p may promote lung adenocarcinoma by targeting SIK1 and may be a potential biomarker for lung cancer.
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