ArticleScientific reports2026
miR-320a enhances radiosensitivity in non-small cell lung cancer by targeting RAD51 and modulating ferroptosis via GPX4.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- MicroRNA-Mediated Regulation of Ionizing Radiation Responses: Mechanisms and Advances in Clinical Translation.Current issues in molecular biology · 2026Review
- Geno-guided targeting of ferroptosis: a multi-layered network to overcome radioresistance in lung cancer.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy is an essential treatment for non-small cell lung cancer (NSCLC), but its effectiveness is often reduced by radioresistance. miR-320a has been shown to improve radiosensitivity in NSCLC, but the molecular mechanisms are not well understood. This study investigates how miR-320a regulates RAD51 to affect the radiosensitivity of NSCLC. miR-320a expression in NSCLC tissues and cell lines was evaluated using The Cancer Genome Atlas (TCGA) data and qRT-PCR. RAD51 was predicted as a miR-320a target using bioinformatic tools (TargetScan, miRDB, miRTarBase) and validated by dual-luciferase reporter assays. Functional experiments were conducted to examine the effects of miR-320a and RAD51 manipulation on NSCLC cell responses to varying radiation doses. Ferroptosis was examined by measuring lipid reactive oxygen species (ROS) and GPX4 expression levels. miR-320a expression was markedly reduced in NSCLC tissues and cell lines relative to normal controls and showed a positive association with clinical radiosensitivity. Functional experiments demonstrated that miR-320a overexpression increased radiosensitivity by inhibiting post-irradiation cell proliferation, colony formation, and migration. RAD51 was validated as a direct post-transcriptional target of miR-320a. Mechanistically, RAD51 expression inversely correlated with miR-320a (R = -0.16, P < 0.001) and was associated with reduced radiosensitivity both in vitro and in patient samples. Importantly, RAD51 knockdown reversed the radioresistance induced by miR-320a inhibition. Further analyses revealed that RAD51 positively regulated GPX4 expression, thereby suppressing ferroptosis. Inhibition of RAD51 or restoration of miR-320a led to enhanced lipid peroxidation, as evidenced by increased lipid ROS accumulation and reduced GPX4 expression, ultimately sensitizing NSCLC cells to radiotherapy. Our results indicate that miR-320a promotes NSCLC radiosensitivity through a negative regulation of RAD51. The miR-320a/RAD51/GPX4 axis may be used as a key pathway in regulating NSCLC radiosensitivity.
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Registered trials
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