Comparative transcriptional profiling of canine acanthomatous ameloblastoma and homology with human ameloblastoma.
Ameloblastoma
/ genetics
Animals
Carcinoma, Squamous Cell
/ metabolism
Dog Diseases
/ genetics
Dogs
Epithelial-Mesenchymal Transition
/ genetics
Gene Expression Profiling
Genes, ras
Gingiva
/ metabolism
Humans
Jaw Neoplasms
/ genetics
MAP Kinase Signaling System
Multigene Family
Mutation
Neoplasm Proteins
/ genetics
Proto-Oncogene Proteins B-raf
/ genetics
Proto-Oncogene Proteins p21(ras)
/ genetics
RNA, Messenger
/ biosynthesis
RNA, Neoplasm
/ biosynthesis
RNA-Seq
Signal Transduction
/ genetics
Species Specificity
Transcriptome
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
07 09 2021
07 09 2021
Historique:
received:
11
05
2021
accepted:
25
08
2021
entrez:
8
9
2021
pubmed:
9
9
2021
medline:
17
11
2021
Statut:
epublish
Résumé
Ameloblastomas are odontogenic tumors that are rare in people but have a relatively high prevalence in dogs. Because canine acanthomatous ameloblastomas (CAA) have clinicopathologic and molecular features in common with human ameloblastomas (AM), spontaneous CAA can serve as a useful translational model of disease. However, the molecular basis of CAA and how it compares to AM are incompletely understood. In this study, we compared the global genomic expression profile of CAA with AM and evaluated its dental origin by using a bulk RNA-seq approach. For these studies, healthy gingiva and canine oral squamous cell carcinoma served as controls. We found that aberrant RAS signaling, and activation of the epithelial-to-mesenchymal transition cellular program are involved in the pathogenesis of CAA, and that CAA is enriched with genes known to be upregulated in AM including those expressed during the early stages of tooth development, suggesting a high level of molecular homology. These results support the model that domestic dogs with spontaneous CAA have potential for pre-clinical assessment of targeted therapeutic modalities against AM.
Identifiants
pubmed: 34493785
doi: 10.1038/s41598-021-97430-0
pii: 10.1038/s41598-021-97430-0
pmc: PMC8423744
doi:
Substances chimiques
Neoplasm Proteins
0
RNA, Messenger
0
RNA, Neoplasm
0
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
Proto-Oncogene Proteins p21(ras)
EC 3.6.5.2
Types de publication
Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17792Subventions
Organisme : NIGMS NIH HHS
ID : R35 GM122575
Pays : United States
Organisme : NIGMS NIH HHS
ID : R24 GM082910
Pays : United States
Informations de copyright
© 2021. The Author(s).
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