ArticleCancer chemotherapy and pharmacology2021
Glaucocalyxin A induces apoptosis and autophagy in tongue squamous cell carcinoma cells by regulating ROS.
Article in Cancer chemotherapy and pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Suppressing CDCA8/CDK1 improves oral squamous cell carcinoma by modulating proliferation, apoptosis, cell cycle and migration.Discover oncology · 2025Article
- Autophagy in oral cancer: Promises and challenges (Review).International journal of molecular medicine · 2024Review
- Identification and validation of autophagy-related genes influenced by paris polyphylla in tongue cancer using network pharmacology.BMC oral health · 2024Article
- Glaucocalyxin A Inhibits the Malignancies of Gastric Cancer Cells by Downregulating MDM2 and RNF6Frontiers in oncology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposeTongue squamous cell carcinoma (TSCC) is the most common highly invasive oral cancer. Glaucocalyxin A (GLA) is a diterpenoid component isolated from Rabdosia japonica var. with anti-bacterial and anti-cancer biological properties. However, the role of GLA in human TSCC remains uncertain. The aim of this paper was to investigate the anti-cancer effect of GLA on TSCC cells as well as its underlying mechanism.
methodsCell viability and growth were analyzed by CCK-8 assay and colony formation, respectively. DAPI staining and flow cytometry assay were used to detect the cell apoptosis. Lysotracker Red staining was used to observe the lysosomes and autolysosomes of TSCC cells. ROS fluorescent probe was used to test the intracellular ROS levels. Western blotting was used to detect the expression levels of apoptosis- and autophagy-related proteins.
resultsGLA inhibits the cell viability and growth in TSCC cells. GLA induces TSCC cells apoptosis, autophagy and ROS production in a time- and concentration-dependent manner. In addition, GLA inhibits the viability of TSCC cells by inducing intracellular ROS production. Finally, GLA triggers ROS-dependent apoptosis and autophagy in TSCC cells.
conclusionOur results consistently suggested that GLA can induce apoptosis and autophagy in TSCC cells by generating ROS. GLA may serve as a promising therapeutic drug for overcoming TSCC.
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