The Role of Vimentin 3 in Ameloblastomas: A Novel Tumor Biomarker


GÜLTEKİN S. E., von Brandenstein M., BARIŞ E., ATAK SEÇEN İ., Arslan Bozdag L., Goebel H.

Oral Diseases, vol.31, no.11, pp.3081-3088, 2025 (SCI-Expanded, Scopus) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 31 Issue: 11
  • Publication Date: 2025
  • Doi Number: 10.1111/odi.15396
  • Journal Name: Oral Diseases
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, CINAHL, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.3081-3088
  • Keywords: ameloblastoma, odontogenic tumor, vimentin 3
  • Gazi University Affiliated: Yes

Abstract

Introduction: Ameloblastoma (ABL), a common odontogenic tumor in the maxillofacial region, presents primarily as unicystic (U-ABL) and conventional (C-ABL) variants. Despite shared epithelial features, their distinct biological behaviors may stem from interactions between connective tissue and epithelial cells. Vimentin 3 (VIM3), a truncated variant of Vimentin-Full Length (VIMFL), exhibits unique biological properties. This study is the first to investigate VIM3 expression in ABLs. Methods: Formalin-fixed paraffin-embedded (FFPE) samples of C-ABL (n = 30), U-ABL (n = 30), and dental follicles (DF, n = 30) were analyzed. Immunohistochemical evaluation of VIM3, VIMFL, WNT5a, and MTCO1 was performed, alongside qRT-PCR for VIM3, VIMFL, WNT5a, ROR2, and miR-498. Results: VIM3 expression was significantly higher in C-ABL (p < 0.0001) compared to U-ABL and DFs. VIMFL was absent in the epithelial components of all cases. C-ABL showed significantly higher WNT5a (p < 0.0001) and MTCO1 (p = 0.0327) expression. qRT-PCR revealed significant differences in VIM3 and miR-498 levels between U-ABL and DFs (p < 0.0001). No significant differences were found for WNT5a, VIMFL, or ROR2 (p > 0.05). Conclusion: This study identifies VIM3 expression in ABLs, distinct from VIMFL, suggesting its potential as a biomarker. Additionally, mitochondrial dysfunction may play a role in ABL tumorigenesis.