RETRACTED: Inhibition of Nasopharyngeal Carcinoma by Beta-Lapachone Occurs by Targeting the Mammalian Target of Rapamycin (mTOR)/PI3K/AKT Pathway, Reactive Oxygen Species (ROS) Production, and Autophagy Induction (Retracted Article)

被引:10
作者
Han, Yongqing [1 ]
Shi, Dayou [2 ]
Li, Jingao [3 ]
机构
[1] Nanchang Univ, Dept Oncol, Nanchang, Jiangxi, Peoples R China
[2] Jiujiang First Peoples Hosp, Dept Oncol, Jiujiang, Jiangxi, Peoples R China
[3] Jiangxi Tumor Hosp, Dept Radiotherapy, Nanchang, Jiangxi, Peoples R China
来源
MEDICAL SCIENCE MONITOR | 2019年 / 25卷
关键词
Autophagy; Cell Migration Assays; Nasopharyngeal Neoplasms; Neoplasm Invasiveness; CELL-CYCLE ARREST; CANCER-CELLS; APOPTOSIS; EPIDEMIOLOGY; ACTIVATION; CISPLATIN;
D O I
10.12659/MSM.915463
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Beta-lapachone has been shown to exhibit potent anti-cancer effects against various cell lines. In the present study, we examined the anti-cancer effects of beta-lapachone, a quinone, against human HNE1 nasopharyngeal carcinoma cells, and also assessed its effects on cellular migration and invasion, autophagy, mTOR/PI3K/AKT signalling pathway, and ROS production. Material/Methods: CCK-8 cell counting assay was used to assess cell viability effects after lapachone treatment. Its effects on the mTOR/PI3K/AKT biochemical pathway were examined by Western blot analysis. Transmission electron microscopy was used to study autophagy induced by beta-lapachone. Effects on cell invasion and cell migration were evaluated by Transwell method. Results: The results revealed that beta-lapachone suppresses the proliferation of HNE1 cells, with an IC50 of 30 mu M. These growth-inhibitory effects of beta-lapachone were found to be dose-dependent. The investigation of the effects of beta-lapachone on the mTOR/PI3KAKT signalling pathway showed that beta-lapachone blocked this pathway in a concentration-dependent manner. Beta-lapachone also inhibited the migration and invasion of HNE1 nasopharyngeal cancer cells, as shown by Transwell assay. The fluorescence microscopy analysis showed that beta-lapachone increased production of reactive oxygen species (ROS), which is also linked with a concentration-dependent decrease in mitochondria) membrane potential (MMP) levels. Electron microscopy analysis showed that beta-lapachone caused the development of the autophagosomes, and the frequency of the autophagosomes increased with increased dosage of beta-lapachone. The beta-lapachone-triggered autophagy was also associated with increased protein levels of LC3 II and decreased levels of p62. Conclusions: The findings of this study suggest that beta-lapachone inhibits the growth of nasopharyngeal cancer cells by promoting autophagy, and it may be useful in cancer drug discovery paradigms.
引用
收藏
页码:8995 / 9002
页数:8
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