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miR-150 inhibits proliferation and tumorigenicity via retarding G1/S phase transition in nasopharyngeal carcinoma

Cancer cells are characterized by a pathological manifestation of uncontrolled proliferation, which results in tumor formation. Therefore, it is necessary to improve understanding of the underlying mechanism of cell cycle control. Here, we report that miR-150 is downregulated in nasopharyngeal carci...

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Detalles Bibliográficos
Autores principales: Li, Xiangyong, Liu, Fumei, Lin, Bihua, Luo, Haiqing, Liu, Meilian, Wu, Jinhua, Li, Caihong, Li, Ronggang, Zhang, Xin, Zhou, Keyuan, Ren, Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5363880/
https://www.ncbi.nlm.nih.gov/pubmed/28350089
http://dx.doi.org/10.3892/ijo.2017.3909
Descripción
Sumario:Cancer cells are characterized by a pathological manifestation of uncontrolled proliferation, which results in tumor formation. Therefore, it is necessary to improve understanding of the underlying mechanism of cell cycle control. Here, we report that miR-150 is downregulated in nasopharyngeal carcinoma tissues and cells. Upregulation of miR-150 suppresses nasopharyngeal carcinoma (NPC) cell proliferation and induces G(1)/S arrest in vitro, and inhibits tumorigenesis in vivo. Conversely, silencing miR-150 yields the opposite effect. Our results further demonstrate that miR-150 retards nasopharyngeal carcinoma cell proliferation and G(1)/S transition via targeting multiple cell cycle-related genes, including CCND1, CCND2, CDK2 and CCNE2. Therefore, our results uncover a novel mechanistic understanding of miR-150-mediated tumor suppression in NPC, which will facilitate the development of effective cancer therapies against nasopharyngeal carcinoma.