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miR-34b inhibits nasopharyngeal carcinoma cell proliferation by targeting ubiquitin-specific peptidase 22

OBJECTIVES: This study aimed to investigate the precise role of miR-34b in nasopharyngeal carcinoma (NPC). MATERIALS AND METHODS: The expression of miR-34b and transcription of ubiquitin-specific peptidase 22 (USP22) were examined using quantitative reverse transcription-polymerase chain reaction. W...

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Detalles Bibliográficos
Autores principales: Xiao, Jianyong, Li, Yingying, Zhang, Wenyin, Jiang, Yanni, Du, Biaoyan, Tan, Yuhui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4803272/
https://www.ncbi.nlm.nih.gov/pubmed/27051294
http://dx.doi.org/10.2147/OTT.S98378
Descripción
Sumario:OBJECTIVES: This study aimed to investigate the precise role of miR-34b in nasopharyngeal carcinoma (NPC). MATERIALS AND METHODS: The expression of miR-34b and transcription of ubiquitin-specific peptidase 22 (USP22) were examined using quantitative reverse transcription-polymerase chain reaction. Western blot analysis was used to measure the protein expression of USP22. A dualluciferase assay was used to investigate the interaction between miR-34b and USP22. Cell viability was determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay. The cell cycle was analyzed by propidium iodide staining followed by flow cytometry analysis. RESULTS: miR-34b was significantly downregulated in NPC tissues and NPC cell lines. Overexpression of miR-34b in NPC SUNE-6-10B cells inhibited cell viability and proliferation. USP22 was highly expressed in NPC cells and promoted cell viability and proliferation. Restoration of USP22 expression could reverse the effect of miR-34b on NPC cell viability and proliferation. CONCLUSION: miR-34b acts as a tumor suppressor in NPC, which is mediated via repression of the oncogene USP22.