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Fibroblast growth factor receptor 1 promotes MG63 cell proliferation and is associated with increased expression of cyclin-dependent kinase 1 in osteosarcoma

Osteosarcoma is the most common type of malignant bone tumor in adolescents and young adults. However, current understanding of osteosarcomagenesis remains limited. In the present study, the role of fibroblast growth factor receptor 1 (FGFR1) in human osteosarcoma cell proliferation was investigated...

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Detalles Bibliográficos
Autores principales: ZHOU, WEI, ZHU, YUE, CHEN, SONG, XU, RUIJUN, WANG, KUNZHENG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686061/
https://www.ncbi.nlm.nih.gov/pubmed/26648125
http://dx.doi.org/10.3892/mmr.2015.4597
Descripción
Sumario:Osteosarcoma is the most common type of malignant bone tumor in adolescents and young adults. However, current understanding of osteosarcomagenesis remains limited. In the present study, the role of fibroblast growth factor receptor 1 (FGFR1) in human osteosarcoma cell proliferation was investigated, and the possible pathways that contribute to FGFR1-mediated osteosarcoma cell proliferation were examined using microarray analysis. The expression of FGFR1 in osteosarcoma tissues was assessed by reverse transcription-quantitative polymerase chain reaction and immunohistochemistry. The results demonstrated that FGFR1 was markedly increased in osteosarcoma tissues, and that the overexpression of FGFR1 in MG63 cells significantly promoted cell proliferation, as observed using the cell viability assay. In addition, FGFR1-mediated cell proliferation was closely associated with cell cycle re-distribution, as determined by microarray analysis. Western blotting identified that the expression of cyclin-dependent kinase 1 (CDK1) was correspondingly increased in response to the overexpression of FGFR1. These results indicated that FGFR1 contributes to cell proliferation in osteosarcoma MG63 cells, and FGFR1 mediated cell proliferation may be attributed to the regulation of the cell cycle regulator, CDK1. These findings provide evidence to support the potential use of molecule target therapy against FGFR1 as a promising strategy in osteosarcoma treatment and prevention.