上海口腔医学 ›› 2023, Vol. 32 ›› Issue (5): 462-467.doi: 10.19439/j.sjos.2023.05.003

• 论著 • 上一篇    下一篇

柯里拉京体内外诱导口腔鳞癌CAL-27细胞凋亡及机制探讨

李胜男1,2, 崔飞艳2, 赵姗2, 杜琛2, 孟箭1,2   

  1. 1.潍坊医学院 口腔医学院,山东 潍坊 261053;
    2.徐州市中心医院 口腔科,江苏 徐州 221000
  • 收稿日期:2022-05-20 修回日期:2022-07-17 出版日期:2023-10-25 发布日期:2023-11-03
  • 通讯作者: 孟箭,E-mail: mrocket@126.com
  • 作者简介:李胜男(1995-),女,在读硕士研究生,医师,E-mail: 18863661105@163.com
  • 基金资助:
    国家口腔疾病临床医学研究中心开放性课题(NCRCO-202101); 徐州市重点研发计划(KC21187)

Corilagin-induced apoptosis of oral squamous carcinoma CAL-27 cells in vitro and in vivo and its mechanism

LI Sheng-nan1,2, CUI Fei-yan2, ZHAO Shan2, DU Chen2, MENG Jian1,2   

  1. 1. School of Stomatology, Weifang Medical University. Weifang 261053, Shandong Province;
    2. Department of Stomatology, Xuzhou Central Hospital. Xuzhou 221000, Jiangsu Province, China
  • Received:2022-05-20 Revised:2022-07-17 Online:2023-10-25 Published:2023-11-03

摘要: 目的:观察柯里拉京(corilagin)对人舌鳞癌CAL-27细胞增殖和凋亡的作用,探讨诱导其凋亡的分子机制。方法:体外实验采用不同浓度的柯里拉京预处理CAL-27细胞,通过CCK-8法及平板克隆形成实验检测细胞增殖能力;流式细胞术检测细胞凋亡;qRT-PCR和Western 印迹法检测对细胞中Bax、Bcl-2、Caspase-3、Cleaved Caspase-3 mRNA及蛋白表达水平的影响。通过CAL-27细胞构建裸鼠移植瘤模型,检测柯里拉京的体内抗肿瘤效果。采用GraphPad Prism 8.0软件包对数据进行统计学分析。结果:体外实验结果显示,柯里拉京以浓度依赖性方式抑制CAL-27细胞增殖,诱导细胞凋亡;在mRNA和蛋白水平上上调Bax、Caspase-3和Cleaved Caspase-3,下调Bcl-2,差异均有统计学意义(P<0.05)。体内实验表明,与对照组相比,柯里拉京组可显著减小裸鼠瘤体体积(P<0.05)。结论:柯里拉京在体内和体外均能显著抑制人舌鳞癌CAL-27细胞增殖并促进其凋亡,其作用机制可能与调控Bax/Bcl-2/Caspase-3信号通路有关。

关键词: 柯里拉京, CAL-27细胞, 增殖, 凋亡, Bax/Bcl-2/Caspase-3信号通路

Abstract: PURPOSE: To investigate the effect of corilagin on proliferation and apoptosis of human oral squamous cell carcinoma CAL-27 cells, and to explore the molecular mechanism of inducing cell apoptosis. METHODS: In vitro experiments, Cal-27 cells were treated with different concentrations of corilagin, cell-counting kit-8(CCK-8) assay and colony formation assay were performed to evaluate cell proliferation; flow cytometric analysis was used to evaluate cell apoptosis; qRT-PCR and Western blot assays were performed to evaluate the effect of corilagin on the expression levels of Bax, Bcl-2, Caspase-3, Cleaved Caspase-3 in CAL-27 cells. In vivo experiments, tumor-bearing nude mice was constructed with CAL-27 cells to evaluate the antitumor effect of corilagin. GraphPad Prism 8.0 software package was used for statistical analysis of the data. RESULTS: In vitro experiments showed that corilagin in a dose-dependent manner inhibited proliferation, induced apoptosis, up-regulated Bax, caspase-3, cleaved caspase-3 and down-regulated Bcl-2 at the mRNA and protein levels of CAL-27 cells, and the differences were statistically significant(P<0.05). In vivo experiments showed that compared with the control group, corilagin could significantly reduce the volume of tumor in nude mice(P<0.05). CONCLUSIONS: Corilagin can significantly inhibit CAL-27 cell growth and promote its apoptosis both in vitro and in vivo, which may be related to the mediation of Bax/Bcl-2/Caspase-3 signaling pathway.

Key words: Corilagin, CAL-27 cells, Proliferation, Apoptosis, Bax/Bcl-2/Caspase-3 signal pathway

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