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MiR-29b suppresses the proliferation and migration of osteosarcoma cells by targeting CDK6
被引:0
|作者:
Kegan Zhu
[1
,2
]
Lei Liu
[3
]
Junliang Zhang
[1
]
Yanbo Wang
[2
]
Hongwei Liang
[2
]
Gentao Fan
[1
]
Zhenhuan Jiang
[3
]
ChenYu Zhang
[2
]
Xi Chen
[2
]
Guangxin Zhou
[1
]
机构:
[1] Department of Orthopedics,School of Medicine,Jinling Hospital,Nanjing University
[2] State Key Laboratory of Pharmaceutical Biotechnology,Collaborative Innovation Center of Chemistry for Life Sciences,NJU Advanced Institute for Life Sciences(NAILS),Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology,School of Life Sc
[3] Department of Orthopedics,The Affiliated Yixing Hospital of Jiangsu
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摘要:
Osteosarcoma is the most common primary sarcoma of bone,and it is a leading cause of cancer death among adolescents and young adults.However,the molecular mechanism underlying osteosarcoma carcinogenesis remains poorly understood.Recently,cyclin-dependent kinase 6(CDK6) was identified as an important oncogene.We found that CDK6 protein level,rather than CDK6 mRNA level,is much higher in osteosarcoma tissues than in normal adjacent tissues,which indicates a post-transcriptional mechanism involved in CDK6 regulation in osteosarcoma.MiRNAs are small noncoding RNAs that repress gene expression at the posttranscriptional level and have widely been shown to play important roles in many human cancers.In this study,we investigated the role of miR-29 b as a novel regulator of CDK6 using bioinformatics methods.We demonstrated that CDK6 can be downregulated by miR-29 b via binding to the 3-UTR region in osteosarcoma cells.Furthermore,we identified an inverse correlation between miR-29 b and CDK6 protein levels in osteosarcoma tissues.Finally,we examined the function of miR-29b-driven repression of CDK6 expression in osteosarcoma cells.The results revealed that miR-29 b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes.Taken together,our results highlight an important role for miR-29 b in the regulation of CDK6 in osteosarcoma and may open new avenues for future osteosarcoma therapies.
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