Por favor, use este identificador para citar o enlazar este ítem: https://doi.org/10.14670/HH-18-637

Título: Targeting eIF5A2 reduces invasion and reverses chemoresistance in SCC-9 cells in vitro
Fecha de publicación: 2024
Editorial: Universidad de Murcia, Departamento de Biologia Celular e Histiologia
Cita bibliográfica: Histology and Histopathology Vol. 39, nº4 (2024)
ISSN: 0213-3911
1699-5848
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Eukaryotic translation initiation factor 5A2
Bim
E-cadherin
Invasion
Apoptosis
Chemotherapy resistance
Oral cancer
Resumen: Background and Aims. Eukaryotic translation initiation factor 5A2 (EIF5A2) has been reported to be involved in metastasis and chemotherapy resistance in many human cancers. However, the effect and mechanism of EIF5A2 in oral cancer cells are unknown. Here, we investigated the effects of targeting EIF5A2 on chemotherapy resistance in oral cancer cells in vitro. Methods. By using a lentiviral system, we investigated the effects of targeting EIF5A2 on the invasion, migration, growth, and chemosensitivity of SCC-9 cells to CDDP in vitro. Through the method of gene intervention, we explore the role of pro-apoptotic Bim and epithelial and mesenchymal marker E-cadherin protein in this process and the regulation of EIF5A2 on Bim and E-cadherin. Results. Targeting EIF5A2 reduces invasion and migration in SCC-9 cells partly through upregulation of E-cadherin expression; Targeting EIF5A2 promotes cell apoptosis and inhibits cell survival as well as increasing chemosensitivity in SCC-9 cells through upregulation of Bim expression. Conclusion. EIF5A2 may be a novel potential therapeutic target for oral cancer by upregulation of Bim and E-cadherin
Autor/es principal/es: Gao, Jinbo
Li, Peng
URI: http://hdl.handle.net/10201/140665
DOI: https://doi.org/10.14670/HH-18-637
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 8
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Aparece en las colecciones:Vol.39, nº4 (2024)

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