ArticleArchives of oral biology2019
Enhanced basal autophagy supports ameloblastoma-derived cell survival and reactivation.
Article in Archives of oral biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth.iScience · 2026Article
- Human Amniotic Mesenchymal Stromal Cells Promote Bone Regeneration via Regulating Ameloblastoma-Derived-Bone Marrow Mesenchymal Cells Crosstalk and Autophagy in Ameloblastoma Microenvironment.Tissue engineering and regenerative medicine · 2026Article
- Time to Recurrence of Ameloblastoma and Associated Factors in a Multi-institutional Black Patient Cohort.Journal of racial and ethnic health disparities · 2025Observational
- Differentially expressed extracellular matrix genes functionally separate ameloblastoma from odontogenic keratocyst.BMC oral health · 2024Article
- Review
- MicroRNA-1-3p Suppresses Malignant Phenotypes of Ameloblastoma Through Down-Regulating Lysosomal Associated Membrane Protein 2-Mediated Autophagy.Frontiers in medicine · 2021Article
- Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 15 (SNHG15) Alleviates Osteoarthritis Progression by Regulation of Extracellular Matrix Homeostasis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivesAmeloblastoma is an aggressive odontogenic jaw neoplasm. Its unlimited growth confers high potential for malignant transformation and recurrence. It is unclear why ameloblastoma is highly recurrent despite surgical resection with a wide margin of normal tissue. While canonical autophagy can be used to degrade and eliminate damaged cellular components, it is also a protective mechanism that provides energy and vital metabolites for cell survival. We used ameloblastoma-derived cells to test the hypothesis that autophagic processes play a role in survival and reactivation of ameloblastoma.
methodsPrimary epithelial (EP-AMCs) and mesenchymal (MS-AMCs) ameloblastoma-derived cells were established from tissue samples of solid multicystic ameloblastoma. Clonogenic capacity and basal autophagic capacity were assessed in ameloblastoma-derived cells relative to human odontoma-derived cells (HODCs) and maxilla-mesenchymal stem cells (MX-MSCs). Ability of ameloblastoma-derived cells to survive and form new ameloblastoma was assessed in mouse tumor xenografts.
resultsEP-AMCs were highly clonogenic (p < 0.0001) and demonstrated enhanced basal levels of autophagic proteins microtubule-associated protein 1-light chain 3 (LC3) (p < 0.01), p62 (Sequestosome 1, SQSTM1) (p < 0.01), and the LC3-adapter, melanoregulin (MREG) (p < 0.05) relative to controls. EP-AMCs xenografts regenerated solid ameloblastoma-like tumor with histological features of columnar ameloblast-like cells, loose stellate reticulum-like cells and regions of cystic degeneration characteristic of follicular variant of solid multicystic ameloblastoma. The xenografts also displayed stromal epithelial invaginations strongly reactive to LC3 and p62 suggestive of epithelial-mesenchymal transition and neoplastic odontogenic epithelium.
conclusionsEP-AMCs exhibit altered autophagic processes that can support survival and recurrence of post-surgical ameloblastoma cells.
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Registered trials
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