ArticleSleep & breathing = Schlaf & Atmung2024
MiR-210-3p enhances intermittent hypoxia-induced tumor progression via inhibition of E2F3.
Article in Sleep & breathing = Schlaf & Atmung, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Circulating microRNAs as Biomarkers of Brain Metastases in Lung Cancer: A Pilot Study.Journal of clinical medicine · 2026Article
- Obstructive sleep apnea and lung cancer: molecular underpinnings and clinical translational prospects.Frontiers in cell and developmental biology · 2026Review
- Obstructive sleep apnea as a modifier of endocrine toxicities associated with immune checkpoint inhibitors in lung cancer.Frontiers in immunology · 2026Review
- The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles.International journal of molecular sciences · 2025Review
- Ginsenoside 20(S)-Rg3 Hinders Esophageal Squamous Cell Carcinoma Cells Malignant Behaviors by miR-210-3p/B4GALT5 Axis.Cell biochemistry and biophysics · 2025Article
- miR-27a-5p, miR-21-5p, miR-1246 and miR-4508: a candidate microRNA signature in the protection and regulation of viral infection in mild COVID-19.Molecular medicine (Cambridge, Mass.) · 2025Article
- PDL1 targeting by miR-138-5p amplifies anti-tumor immunity and Jurkat cells survival in non-small cell lung cancer.Scientific reports · 2024Article
- Impact of Hypoxia-Induced miR-210 on Pancreatic Cancer.Current issues in molecular biology · 2023Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
purposeIntermittent hypoxia (IH) is a hallmark of obstructive sleep apnea (OSA), which is related to tumorigenesis and progression. Although micro-ribonucleic acid-210-3p (miR-210-3p) is correlated with hypoxia-induced tumor development, its role in the relationship between IH and tumor function remains poorly understood. The present work focused on elucidating the molecular mechanism through which miR-210-3p drives tumor progression under IH.
methodsMiR-210-3p levels were quantified within tumor samples from patients with lung adenocarcinoma who had or did not have OSA. Correlations between miR-210-3p and polysomnographic variables were analyzed. For in vitro experiments, miR-210-3p was inhibited or overexpressed via transfection under IH conditions. Cell viability, growth, invasion and migration assays were carried out. For in vivo modeling of IH using mouse xenografts, a miR-210-3p antagomir was intratumorally injected, tumor biological behaviors were evaluated, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry and western blot were carried out for detecting miR-210-3p and E2F transcription factor 3 (E2F3) expression.
resultsFor patients with lung adenocarcinoma and OSA, high miR-210-3p levels showed positive relation to polysomnographic variables, such as oxygen desaturation index, apnea-hypopnea index, and proportion of total sleep time with oxygen saturation in arterial blood < 90%. IH enhanced tumor viability, proliferation, migration, and invasion, downregulated E2F3 expression, and increased miR-210-3-p levels. miR-210-3p overexpression induced similar changes. These changes were reversed by miR-210-3p inhibition in vitro or miR-210-3p antagomir through intratumoral injection in vivo.
conclusionsIH-induced tumor development is driven through miR-210-3p by E2F3 suppression. MiR-210-3p represents a potential therapeutic target among patients with concomitant cancer and OSA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.