ArticleJournal of oral and maxillofacial pathology : JOMFP
Deoxyelephantopin induces cell death in oral cancer cells via the downregulation of AKT1-mTOR-mediated mechanisms.
Article in Journal of oral and maxillofacial pathology : JOMFP. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Jaceidin Inhibits Proliferation and Promotes Apoptosis in Oral Squamous Cell Carcinoma Cells by Regulating Survivin and AKT/ERK Signaling Pathways.International journal of molecular sciences · 2026Article
- Pharmacological insights into deoxyelephantopin: a multifunctional sesquiterpene with therapeutic promise in cancer and neurodegenerative disorders.Molecular biology reports · 2026Review
- SFXN1 expression analysis in oral squamous cell carcinoma and its association with the PI3K-AKT-mTOR pathway and immune cell infiltration.Journal of oral biology and craniofacial researchArticle
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2 authors.
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Abstract
Background: Oral cancer, particularly oral squamous cell carcinoma (OSCC), is a prevalent malignancy in Southeast Asia with low survival rates. Deoxyelephantopin (DET), a natural compound derived from Aim: By focussing on the AKT1/mTOR signalling pathway, which controls tumour cell proliferation and survival, this study explores the molecular underpinnings behind DET's therapeutic potential in OSCC. Materials and Methods: Results: The MTT assay showed that DET inhibited KB oral cancer cell growth in a dose-dependent manner, increasing oxidative stress and reducing superoxide dismutase (SOD) and catalase (CAT) activities. RT-PCR revealed a shift in gene expression, with upregulation of pro-apoptotic genes (BAX, CASP-3, CASP-6, and CASP-9) and downregulation of anti-apoptotic genes, confirming mTOR pathway inhibition. Molecular docking indicated strong binding affinities between DET and key apoptotic and survival proteins. MD simulations showed strong stability for protein target against DET. Conclusions: DET effectively disrupts AKT1/mTOR signalling, inducing apoptosis and oxidative stress in OSCC cells. Its high biocompatibility (SWISS-ADME) and strong molecular interactions support its potential as a novel therapeutic agent for OSCC. This integrative approach provides valuable insights into DET's mechanism of action, paving the way for pre-clinical and clinical applications.
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