Publication: Expression of ALKBH5 in Odontogenic Lesions
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0
Issued Date
2025-01-01
Resource Type
ISSN
15412016
eISSN
15334058
Scopus ID
2-s2.0-85209691623
Pubmed ID
39523879
Journal Title
Applied Immunohistochemistry and Molecular Morphology
Volume
33
Issue
1
Start Page
49
End Page
57
Rights Holder(s)
SCOPUS
Bibliographic Citation
Applied Immunohistochemistry and Molecular Morphology Vol.33 No.1 (2025) , 49-57
Suggested Citation
Udompatanakorn C., Sriphongphankul W., Taebunpakul P. Expression of ALKBH5 in Odontogenic Lesions. Applied Immunohistochemistry and Molecular Morphology Vol.33 No.1 (2025) , 49-57. 57. doi:10.1097/PAI.0000000000001233 Retrieved from: https://hdl.handle.net/20.500.14740/20279
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Abstract
N6-methyladenosine (m6A) is the most abundant epigenetic RNA modification in eukaryotes and plays a role in various cancers in humans. This m6A modification is regulated by m6A writers, erasers, and readers. One of the m6A erasers is α-ketoglutarate-dependent dioxygenase homolog 5 (ALKBH5). Previous studies have suggested that ALKBH5 is involved in the pathogenesis of head and neck squamous cell carcinoma. However, the role of ALKBH5 in odontogenic lesions has never been investigated. This study aimed to examine ALKBH5 expression in dental follicles (DFs), dentigerous cysts (DCs), odontogenic keratocyst (OKC), and ameloblastoma (AM) using immunohistochemistry. Six cases of DF, 20 cases of DC and OKC, respectively, and 30 cases of AM were included. The expression patterns, percentage of ALKBH5-positive cells, staining intensities, and immunoreactive scores were examined. ALKBH5 was mainly expressed in the nuclei of the epithelial cells in odontogenic lesions. The percentage of ALKBH5-positive cells was significantly higher in OKC and AM samples compared with DF samples (P < 0.01). The percentage of ALKBH5-positive cells was also higher in OKC and AM samples than in DC samples; however, these results did not show statistical significance (P > 0.05). ALKBH5 cell staining intensities and immunoreactive scores were significantly greater in OKC and AM samples than in DF and DC samples (P < 0.01). Our results suggested that ALKBH5 might play a role in the pathogenesis of odontogenic lesions. Further investigation is needed to elucidate the precise molecular mechanism of the role of ALKBH5 in these diseases.
