中文摘要：

Osteosarcoma 是骨头的最普通的主要肉瘤，并且它是在青少年和年轻成年人之中的癌症死亡的一个领先的原因。然而，糟糕位于 osteosarcoma carcinogenesis 遗体下面的分子的机制理解。最近， cyclin 依赖的 kinase (CDK6 ) 6 作为重要 oncogene 被识别。我们发现了那 CDK6 蛋白质水平，而非 CDK6 mRNA 水平，比的在 osteosarcoma 纸巾是高得多的在正常邻近的纸巾，它显示在 osteosarcoma 涉及 CDK6 规定的 post-transcriptional 机制。MiRNAs 是镇压的小非编码的 RNA 在 post-transcriptional 水平的基因表示并且广泛地被显示了在许多人的癌症起重要作用。在这研究，我们用生物信息学方法作为 CDK6 的一个新奇管理者调查了 miR-29b 的角色。我们证明 CDK6 能是由经由到在 osteosarcoma 房间的 3-UTR 区域的绑定的 miR-29b 的 downregulated。而且，我们在 osteosarcoma 纸巾识别了在 miR-29b 和 CDK6 蛋白质层次之间的反的关联。最后，我们在 osteosarcoma 房间检验了 CDK6 表示的 miR-29b-driven 压抑的功能。结果表明 miR-29b 由在增长和移植进程指向 CDK6 充当 osteosarcoma 的肿瘤 suppressor。一起拿，我们的结果在 osteosarcoma 在 CDK6 的规定为 miR-29b 加亮一个重要角色并且可以为未来 osteosarcoma 治疗打开新大街。

英文摘要：

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 onco- gene. 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 non- coding RNAs that repress gene expression at the post- transcriptional level and have widely been shown to play important roles in many human cancers. In this study, we investigated the role of miR-29b as a novel regulator of CDK6 using bioinformatics methods. We demon- strated that CDK6 can be downregulated by miR-29b via binding to the 3＇-UTR region in osteosarcoma cells. Furthermore, we identified an inverse correlation between miR-29b and CDK6 protein levels in osteosar- coma tissues. Finally, we examined the function of miR- 29b-driven repression of CDK6 expression in osteosarcoma cells. The results revealed that miR-29b 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-29b in the regulation of CDK6 in osteosarcoma and may open new avenues for future osteosarcoma therapies.