Modulation Of Nf-Κb Expression In Esophageal Cancer Cells by Andrographolide and Combined Effects With Radiotherapy

Background: Esophageal cancer (EC) maintains a visible disease burden in China, constituting a major public health challenge among gastrointestinal malignancies, with limitations in the efficacy of existing single-treatment modalities. Andrographolide, a natural active component, has yet to have its radiosensitizing mechanisms fully elucidated. Objectives: This article was designed to elucidate Andrographolide’s synergistic inhibition with radiotherapy and its molecular basis on human esophageal squamous cell carcinoma (EC9706) cells. Methods: Using EC9706, cell proliferation was detected by the CCK-8 assay (at 24/48/72 h), migration ability was assessed by the scratch assay (at 12/24/48 h), radiosensitivity was analyzed by the colony formation (CF) assay (at 0-6 Gy), and the level of associated proteins was subjected to detection by Western blot (WB). Results: The combination group (DG) suggested the strongest proliferation inhibition at all time points [vs. control group (AG)], with the most visible distinction at 72 h. The scratch healing rate was the lowest (at 48 h vs. AG) (P < 0.01). As the radiation dose increased, the CF rate (CFR) declined markedly (6 Gy vs. AG, P < 0.001). Molecular detection revealed that the DG had the highest expression of Cleaved Caspase-3 and Bax, and the lowest expression of Bcl-2, NF-κB p65, and p-IκBα (P < 0.01). Conclusion: Andrographolide enhances the radiosensitivity of EC cells by activating apoptosis pathways and inhibiting the NF-κB signaling pathway, providing experimental evidence for clinical combined treatment.