Curcumin potentiates laryngeal squamous carcinoma radiosensitivity via NF-KB inhibition by suppressin IKKγ expression

Context: Curcumin has shown efficacy in promoting radiosensitivity combined with radiotherapy. However, the role and mechanism of curcumin on radiosensitivity in laryngeal squamous cell cancer (LSCC) is largely unknown. Objective: The aim of our study is to explore the role of IKK gamma-NF-kappa B signaling in curcumin enhancing LSCC cell radiosensitivity in vitro. Materials and methods: Curcumin and X-ray were used to induce cell DNA damage and apoptosis, or inhibit cell clone formation. IKK gamma siRNA and plasmid were used to change IKK gamma expression. The CCK8 assay was used to detect cell viability. Clone formation ability was analyzed using a clonogenic assay, cell apoptosis was examined using flow cytometry, an immunofluorescence assay was used to detect DNA damage, while mRNA and protein levels were assayed using real time PCR and western blotting, respectively. Results: Curcumin significantly enhanced irradiation-induced DNA damage and apoptosis, while weak-ening clone-forming abilities of LSCC cell line Hep2 and Hep2-max. Compared to Hep2 cells, Hep2-max cells are more sensitive to curcumin post-irradiation. Curcumin suppressed irradiation-induced NF-kappa B activation by suppressing IKK gamma expression, but not IKKa and IKK gamma. Overexpression of IKK gamma decreased irradiation-induced DNA damage and apoptosis, while promoting clone-forming abilities of Hep2 and Hep2-max cells. IKK gamma overexpression further increased expression of NF-kappa B downstream genes, Bcl-XL, Bcl-2, and cyclin D1. Conversely, IKK gamma silencing enhanced irradiation-induced DNA dam-age and apoptosis, but promoted clone formation in Hep2 and Hep2-max cells. Additionally, IKK gamma silencing inhibited expression of Bcl-XL, Bcl-2, and cyclin D1. Conclusions: Curcumin enhances LSCC radiosensitivity via NF-kappa B inhibition by suppressing IKK gamma expression.