Department of Biomedical Science and Environmental Biology, Ph.D. Program in Life Sciences, College of Life Sciences, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.
Int J Mol Sci. 2022 Mar 10;23(6):2981. doi: 10.3390/ijms23062981.
Cryptocaryone (CPC) was previously reported as preferential for killing natural products in oral cancer cells. However, its radiosensitizing potential combined with ultraviolet C (UVC) cell killing of oral cancer cells remains unclear. This study evaluates the combined anti-proliferation effect and clarifies the mechanism of combined UVC/CPC effects on oral cancer cells. UVC/CPC shows higher anti-proliferation than individual and control treatments in a low cytotoxic environment on normal oral cells. Mechanistically, combined UVC/CPC generates high levels of reactive oxygen species and induces mitochondrial dysfunction by generating mitochondrial superoxide, increasing mitochondrial mass and causing the potential destruction of the mitochondrial membrane compared to individual treatments. Moreover, combined UVC/CPC causes higher G2/M arrest and triggers apoptosis, with greater evidence of cell cycle disturbance, annexin V, pancaspase, caspases 3/7 expression or activity in oral cancer cells than individual treatments. Western blotting further indicates that UVC/CPC induces overexpression for cleaved types of poly (ADP-ribose) polymerase and caspase 3 more than individual treatments. Additionally, UVC/CPC highly induces γH2AX and 8-hydroxy-2'-deoxyguanosine adducts as DNA damage in oral cancer cells. Taken together, CPC shows a radiosensitizing anti-proliferation effect on UVC irradiated oral cancer cells with combined effects through oxidative stress, apoptosis and DNA damage.
Cryptocaryone (CPC) 先前被报道为对口腔癌细胞中天然产物具有选择性杀伤作用。然而,其与紫外线 C (UVC) 联合杀伤口腔癌细胞的放射增敏潜力尚不清楚。本研究评估了联合 UVC/CPC 对口腔癌细胞的增殖抑制作用,并阐明了其作用机制。在低细胞毒性环境下,UVC/CPC 联合处理对正常口腔细胞的增殖抑制作用明显高于单独处理和对照组。从机制上看,与单独处理相比,联合 UVC/CPC 产生高水平的活性氧,并通过生成线粒体超氧阴离子诱导线粒体功能障碍,增加线粒体质量,并可能破坏线粒体膜。此外,联合 UVC/CPC 导致更高的 G2/M 期阻滞并引发细胞凋亡,与单独处理相比,在口腔癌细胞中表现出更明显的细胞周期紊乱、膜联蛋白 V、多聚半胱氨酸蛋白酶、半胱氨酸蛋白酶 3/7 的表达或活性。Western blot 进一步表明,与单独处理相比,UVC/CPC 诱导的聚(ADP-核糖)聚合酶和胱天蛋白酶 3 的裂解型表达更高。此外,UVC/CPC 可高度诱导口腔癌细胞中的 γH2AX 和 8-羟基-2'-脱氧鸟苷加合物作为 DNA 损伤。综上所述,CPC 对 UVC 照射的口腔癌细胞具有放射增敏的增殖抑制作用,其联合作用通过氧化应激、细胞凋亡和 DNA 损伤发挥作用。