Costunolide enhances cisplatin-induced cytotoxicity in hypopharyngeal SCC FaDu cells by increasing the production of reactive oxygen species

• Published in: Pathology, research and practice research and practice, 2022-08, Vol.236, p.153966-153966, Article 153966
• Main Authors: Li, Juedan, Duan, Baojun, Cheng, Zheng, Kou, Mingqing
• Format: Article
• Language: English
• Subjects: AKT; Apoptosis; Costunolide; HSCC; NF-κB; ROS
• ISSN: 0344-0338; 1618-0631
• DOI: 10.1016/j.prp.2022.153966

The sesquiterpene lactone costunolide (CTL) has attracted much attention due to its antitumor effect on a variety of malignant tumors. However, the effect of CTL on hypopharyngeal squamous cell carcinoma (HSCC) remains unclear. This study aimed to examine the effects of this sesquiterpene lactone on HSCC FaDu cells. The FaDu cell line was treated with CTL and/or cisplatin. CCK-8 was used to examine cell viability. Annexin-FITC/PI and Hoechst 33258 staining were used to measure apoptosis. Reactive oxygen species (ROS) were analysed by MitoSOX Red staining. Protein expression was examined by Western blotting. CTL (0, 2, 4, 6, 8, 10, 20, 30, and 40 µM) dose-dependently induced cytotoxicity in FaDu cells. CTL increased ROS production and induced apoptosis in FaDu cells. Moreover, CTL synergized with cisplatin to induce apoptosis in FaDu cells. In addition, the caspase inhibitor Z-DEVD-FMK attenuated CTL-induced apoptosis. Western blot analysis showed that CTL increased the expression levels of cleaved caspase-3 and Bax and decreased the expression levels of Bcl-2, phospho-AKT and phospho-NF-κB. In conclusion, these data demonstrate that CTL induced apoptosis and enhanced cisplatin-induced cytotoxicity in HSCC FaDu cells.