Correction: Osthole Promotes Cell Senescence-Like Phenotype to Enhance Radiosensitivity in Non-Small Cell Lung Carcinoma Possibly Through Modulating the Sirt1/NF-κB Pathway

Radioresistance is a major problem in non-small cell lung carcinoma (NSCLC) treatment. Osthole is a natural coumarin with antitumor effects. This research sought to clarify if Osthole enhances the sensitivity of NSCLC to radiotherapy and to uncover the underlying mechanisms involved. Cell Counting Kit-8 (CCK-8) assay evaluated the impact of Osthole on the viability of BEAS-2B as well as NSCLC cells, and evaluated the combined effect of different Ionizing radiation (IR) doses with Osthole in order to screen for the appropriate treatment concentration. The malignant biology of NSCLC cells was determined using Scratch-wound assay, clone formation, transwell assay and flow cytometry. To evaluate cellular senescence, SA-β-Gal staining was utilized, and the concentrations of senescence-related cytokines were analyzed using ELISA kits. A model of subcutaneous tumors was developed using nude mice, followed by pathological staining to assess cell growth, apoptosis and changes in indicator protein expression. Western blot evaluated the expression levels of Sirt1/NF-κB pathway, apoptosis, cell cycle and cellular senescence related proteins. Osthole at 40 μM showed no notable influence on BEAS-2B cell viability, but could reduce the viability and clone formation ability of NSCLC cells, hindered their migration and invasion, and triggered apoptosis. Co-treatment of Osthole with IR increased the suppressive effect of IR on the malignant biology of NSCLC cells, and also blocked cells in G1 phase and induced senescence-related marker changes. Furthermore, Osthole modulated the Sirt1/NF-κB pathway, and the Sirt1 agonist SRT1720 alleviated Osthole-induced cell senescence-like phenotype and apoptosis. Osthole treatment reduced the volume and mass of tumor tissue, inhibited cell proliferation and promoted apoptosis. Notably, Osthole also modulated Sirt1/NF-κB pathway and induced cell senescence-like phenotype in vivo. Osthole increases the radiosensitivity of NSCLC cells and promotes cell senescence-like phenotype and G1-phase blockade possibly through modulating Sirt1/NF-κB pathway. Osthole enhances the responsiveness of NSCLC cells to radiotherapy, promotes cell senescence-like phenotype and apoptosis possibly via modulating Sirt1/NF-κB pathway, thus effectively inhibits the malignant progression of NSCLC.