补骨脂乙素对鼻咽癌细胞增殖和凋亡的影响及其机制

Effect of isobavachalcone on proliferation and apoptosis of human nasopharyngeal carcinoma cells and its mechanism

目的观察补骨脂乙素(IBC)对鼻咽癌CNE-2Z细胞增殖和凋亡的影响,并探讨其作用机制。方法采用CCK-8法检测不同浓度IBC对CNE-2Z细胞活性的抑制作用;Ed U掺入法检测细胞增殖能力的改变;平板克隆形成实验检测对CNE-2Z细胞克隆形成能力的影响;流式细胞术Annexin VFITC/PI双染法检测细胞凋亡情况;Western blot检测IBC作用后磷酸化核糖体S6激酶2(p-RSK2)、核糖体S6激酶2(RSK2)、c-Jun、B淋巴细胞瘤/白血病-2(Bcl-2)和Bcl-2相关X蛋白(Bax)表达的改变。结果 IBC对CNE-2Z细胞生长、增殖和克隆形成能力有明显的抑制作用,呈剂量依赖关系;与对照组相比,20、40μmol/L IBC处理组细胞的凋亡率显著增高;IBC可引起CNE-2Z细胞中p-RSK2、c-Jun和Bcl-2表达明显减少,而Bax表达增高,与对照组相比,20、40μmol/L IBC处理组Bcl-2/Bax比值分别下调47.24%和69.50%。结论 IBC可明显抑制鼻咽癌CNE-2Z细胞的增殖,并诱导其凋亡,其机制可能与抑制RSK2活性,进而调控c-Jun和Bcl-2/Bax的表达有关。

Objective To observe the effect of isobavachalcone （IBC） on proliferation and apoptosis of human nasopharyngeal carcinoma （NPC） CNE2Z cells, and explore its mechanism. Methods CNE-2Z cells were treated with various concentrations of IBC, and then the ability of cell growth, proliferation, and colony formation were detected by CCK-8 assay, 5-ethynyl-2＇-deoxyuridine incorporation assay, and colony-formlng assay, respectively. Cell apoptosis was detected by flow cytometry with AnnexinV-FITC/PI double-staining method. Western blot assay was used to detect the expression of phospho-ribosomal S6 kinase 2 （p-RSK2） , ribosomal S6 kinase 2 （RSK2） , c- Jun, B-cell leukemia/lymphoma 2 （Bcl-2）, and Bcl-2-assoeiated X protein （Bax）. Results The growth, prolif- eration and colony formation of CNE-2Z cells were inhibited by treatment with IBC in a concentration-dependent manner. Compared with control group, cell apoptotic ratios were significantly increased in 20 and 40 μmol/L IBC- treated groups. The expression of p-RSK2, c-Jun and Bcl-2 was markedly decreased by treatment with IBC, and the level of Bax was up-regulated. Compared with control group, the ratios of Bcl-2/Bax were respectively decreased by 47.24% and 69.50% in 20 and 40 μmol/L IBC-treated groups. Conclusion IBC could effectively suppress proliferation and induce apoptosis in CNE-2Z cells, which may contribute to regulating RSK2-mediated c- Jun and Bcl-2/Bax pathways.