ArticleMedical science monitor : international medical journal of experimental and clinical research2019
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.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting the Interplay of Autophagy and ROS for Cancer Therapy: An Updated Overview on Phytochemicals.Pharmaceuticals (Basel, Switzerland) · 2023Review
- X-ray repair cross-complementing protein 1 (XRCC1) loss promotes β-lapachone -induced apoptosis in pancreatic cancer cells.BMC cancer · 2021Article
- Autophagy-related signaling pathways are involved in cancer (Review).Experimental and therapeutic medicine · 2021Review
- 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.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
Corrections and comments
- Retraction · 2021-03-11Lack of Approval from Author ·
- Retracted
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 AND 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 µM. 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 mitochondrial 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.
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