ArticleCancer biology & medicine2024
MicroRNA-384 radiosensitizes human non-small cell lung cancer by impairing DNA damage response and repair signaling, which is inhibited by NF-κB.
Article in Cancer biology & medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- MicroRNA-Mediated Regulation of Ionizing Radiation Responses: Mechanisms and Advances in Clinical Translation.Current issues in molecular biology · 2026Review
- Exosomes and lung cancer: Biogenesis, pathogenic mechanisms, biomarkers, and therapeutic applications.The Journal of international medical research · 2026Review
- Integrating Single-Cell, Bulk, and Spatial Transcriptomics Unveils a Novel Ribosome Biogenesis-Related Prognostic Model and DefinesInternational journal of molecular sciences · 2026Article
- MicroRNA-regulated signaling and tumor microenvironment modulation in lung cancer: mechanistic insights and translational opportunities.Cancer cell international · 2026Review
- Metal Nanoparticles as Sensitizers in Energy-Based Therapies for Lung Cancer: From Mechanistic Insights to Clinical Translation.International journal of nanomedicine · 2026Review
- Mechanisms Underlying Radioresistance and Reversal Strategies in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2025Review
- Targeting DNA Damage Response-Mediated Resistance in Non-Small Cell Lung Cancer: From Mechanistic Insights to Drug Development.Current oncology (Toronto, Ont.) · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
objectiveRadiotherapy has achieved remarkable effects in treating non-small cell lung cancer (NSCLC). However, radioresistance remains the major obstacle to achieving good outcomes. This study aims at identifying potential targets for radiosensitizing NSCLC and elucidating the underlying mechanisms.
methodsLentivirus-based infection and CRISPR/Cas9 technology were used to modulate the expression of microRNA-384 (miR-384). Cell clonogenic formation assays and a xenograft tumor model were used to analyze radiosensitivity in NSCLC cells. Fluorescence-activated cell sorting was used to assess the cell cycle and cell death. Immunofluorescence staining, Comet assays, and homologous recombination or non-homologous end-joining I-SceI/GFP reporter assays were used to study DNA damage and repair. Western blotting and quantitative real-time polymerase chain reaction were used to identify the targets of miR-384. Chromatin immunoprecipitation and polymerase chain reaction were performed to evaluate upstream regulators of miR-384.
resultsMiR-384 was downregulated in NSCLC. Overexpression of miR-384 increased the radiosensitivity of NSCLC cells
conclusionsMiR-384 is an ionizing radiation-responsive gene repressed by NF-κB. MiR-384 enhances the radiosensitivity of NSCLC cells
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What Socratic holds
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 Socratic graph.