Head & Neck · 2020 · 25 citations · 51 references
MedicineCancer BiologyOncologyCarcinogenesisMolecular OncologyOral OncologyCancer Stem Cell MaintenanceCancer Stem CellsInvasion In Oral CancerOral CarcinogenesisOral NeoplasiaSquamous Cell CarcinomaCancer Stem Cell Signaling PathwaysCancer Stem Cell-mediated ResistanceChemotherapy For Oral CancerOral Carcinogenesis PromotionPluripotency Transcription NetworksStemness RegulationTherapy-resistant Cancer Stem CellsTranscription Factors In Pluripotency
BACKGROUND: Cisplatin-resistant oral squamous cell carcinoma (OSCC) cells acquire stem-like characteristics and are difficult to treat. Nanog is a transcription factor and needed for maintenance of pluripotency, but its transcription-promoting role in OSCC progression and cisplatin resistance is poorly understood. METHODS: )/chemoradiation-resistant OSCC samples, cisplatin-resistant (CisR-SCC-4/-9) OSCC cells/parental cells, photochemical ECGC, and siRNA (Nanog) were used. RESULTS: Nanog overexpression was associated with overall progression, chemoresistance, and invasion of OSCC. Nanog recruitment to c-Myc, Slug, E-cadherin, and Oct-4 gene promoter was observed. Positive correlation of Nanog protein expression with c-Myc, Slug, cyclin D1, MMP-2/-9, and Oct-4 and negative correlation with E-cadherin gene expression were found. Knockdown of Nanog and treatment of epicatechin-3-gallate reversed cisplatin resistance and diminished invasion/migration potential. CONCLUSION: Nanog directly participated in the regulation of Slug, E-cadherin, Oct-4, and c-Myc genes, causing cisplatin resistance/recurrence of OSCC.
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