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• W2748329577 abstract "Abstract Oral squamous cell carcinoma ( OSCC ) develops through a multistep carcinogenic process involving field cancerization. The DEK gene is a proto‐oncogene with functions in genetic and epigenetic modifications, and has oncogenic functions, including cellular proliferation, differentiation, and senescence. DEK overexpression is associated with malignancies; however, the functional roles of DEK overexpression are unclear. We demonstrated that DEK ‐expressing cells were significantly increased in human dysplasia/carcinoma in situ and OSCC . Furthermore, we generated ubiquitous and squamous cell‐specific doxycycline ( DOX )‐inducible Dek mice ( iD ek and iD ek‐e mice respectively). Both DOX + iD ek and iD ek‐e mice did not show differences in the oral mucosa compared with DOX ‐ mice. In the environment exposed to carcinogen, DOX ‐treated ( DOX +) iD ek mice showed field cancerization and OSCC development. Microarray analysis revealed that DEK overexpression was mediated by the upregulation of DNA replication‐ and cell cycle‐related genes, particularly those related to the G 1 / S transition. Tongue tumors overexpressing DEK showed increased proliferating cell nuclear antigen and elongator complex protein 3 expression. Our data suggest that DEK overexpression enhanced carcinogenesis, including field cancerization, in OSCC by stimulating the G 1 / S phase transition and promoting DNA replication, providing important insights into the potential applications of DEK as a target in the treatment and prevention of OSCC." @default.
• W2748329577 created "2017-08-31" @default.
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• W2748329577 date "2017-08-23" @default.
• W2748329577 modified "2023-10-16" @default.
• W2748329577 title "Promotion of cell proliferation by the proto-oncogene<i>DEK</i>enhances oral squamous cell carcinogenesis through field cancerization" @default.
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• W2748329577 doi "https://doi.org/10.1002/cam4.1157" @default.
• W2748329577 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5633549" @default.
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