Institute of Translational Medicine, the First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Department of Clinical Pharmacy and Pharmaceutical Management, School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.
Oncol Rep. 2017 Aug;38(2):1233-1239. doi: 10.3892/or.2017.5779. Epub 2017 Jul 3.
The function of sodium cantharidinate on inducing hepatocellular carcinoma cell apoptosis was investigated for the first time. Sodium cantharidinate inhibits HepG2 cell growth mainly by LC3 autophagy pathway. MTT results show that sodium cantharidinate effectively inhibits the proliferation of HepG2 cells in a dose- and time-dependent manner and induce cell apoptosis by caspase-3 activity. The further western blotting and FACS detection show that sodium cantharidinate initiates HepG2 cell autophagy program by LC3 pathway. Autophagy-specific inhibitor 3-MA reduce sodium cantharidinate-induced caspase-3 activity and HepG2 cell apoptosis. Silence of the LC3 gene in HepG2 cell lines also reduce sodium cantharidinate-induced cell apoptosis. Collectively, our data indicate that sodium cantharidinate induces HepG2 cell apoptosis through LC3 autophagy pathway. Sodium cantharidinate has potential for development as a new drug for treatment of human HCC.
首次研究了斑蝥酸钠诱导肝癌细胞凋亡的作用。斑蝥酸钠主要通过 LC3 自噬途径抑制 HepG2 细胞生长。MTT 结果表明，斑蝥酸钠能有效抑制 HepG2 细胞的增殖，呈剂量和时间依赖性，并通过 caspase-3 活性诱导细胞凋亡。进一步的 Western blot 和 FACS 检测表明，斑蝥酸钠通过 LC3 途径启动 HepG2 细胞自噬程序。自噬特异性抑制剂 3-MA 降低斑蝥酸钠诱导的 caspase-3 活性和 HepG2 细胞凋亡。沉默 HepG2 细胞系中的 LC3 基因也降低了斑蝥酸钠诱导的细胞凋亡。综上所述，我们的数据表明，斑蝥酸钠通过 LC3 自噬途径诱导 HepG2 细胞凋亡。斑蝥酸钠具有作为治疗人 HCC 的新药的开发潜力。
