Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway

被引:30
作者
Zhang, Yong [1 ]
Weng, Qiuyan [2 ]
Han, Jinming [3 ]
Chen, Jianming [1 ]
机构
[1] Ningbo 6 Hosp, Dept Trauma Orthoped, 1059 Zhongshan Dong Rd, Ningbo 315000, Zhejiang, Peoples R China
[2] Ningbo Univ, Affiliated Hosp, Dept Neurol, Med Sch, Ningbo 315000, Zhejiang, Peoples R China
[3] Ningbo 6 Hosp, Dept Spinal Surg, Ningbo 315000, Zhejiang, Peoples R China
关键词
alantolactone; osteosarcoma; PI3K; AKT; therapy; NF-KAPPA-B; MATRIX METALLOPROTEINASES; CYCLIN D1; DOWN-REGULATION; CELL INVASION; BONE SARCOMA; APOPTOSIS; ACTIVATION; INHIBITION; EXPRESSION;
D O I
10.3892/mmr.2019.10882
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Osteosarcoma is the most common type of malignant bone cancer and results in cancer-related deaths among adolescents. Alantolactone (ALT) demonstrates antitumor properties in various diseases; however, its potential role in osteosarcoma is relatively unclear. The aim of the present study was to evaluate the effect of ALT on osteosarcoma. ALT significantly decreased the viability of U2OS and HOS osteosarcoma cell lines. Cells flow cytometry assay and Hoechst 33258 staining assay revealed that ALT significantly increased the proportion of apoptotic U2OS cells. In addition, wound healing and Transwell invasion assays demonstrated that the invasion and migration of osteosarcoma were markedly reduced upon ALT treatment. It was hypothesized that the antitumor functions of ALT are mediated through inhibition of the PI3K/AKT signaling pathway. In conclusion, the results of the present study confirmed the inhibition of ALT on osteosarcoma cells via downregulation of PI3K/AKT signaling pathways, suggesting ALT as a potential therapeutic candidate for osteosarcoma.
引用
收藏
页码:675 / 684
页数:10
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