Notch-1 promotes the malignant progression of osteosarcoma through the activation of cell division cycle 20.
Notch-1 promotes the malignant progression of osteosarcoma through the activation of cell division cycle 20.
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DOI：
10.18632/aging.202314
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发表时间：
2020-12-19
期刊：
影响因子：
--
通讯作者：
Shang G
中科院分区：
文献类型：
--
作者：
Gao Y;Bai L;Shang G
骨肉瘤（OS）发病机制的分子机制知之甚少。Notch信号通路已被证明是至关重要的参与肿瘤的发生，包括OS。因此，我们探讨了Notch-1信号通路参与OS进展的分子机制。进行了几种方法来确定Notch-1在OS细胞中的生物学功能。MTT结果显示，Notch-1过表达增加OS细胞的活力，而Notch-1下调降低细胞活力。因此，Notch-1的调控可调节OS细胞的凋亡和迁移侵袭能力.机制研究表明，Notch-1过表达增强了OS细胞中细胞分裂周期20（Cdc 20）的表达。此外，Cdc 20过表达可减轻Notch-1下调对OS细胞存活、迁移和侵袭的抑制作用。我们的研究通过抑制Notch-1提供了一种有希望的OS治疗策略。
The molecular mechanism of osteosarcoma (OS) pathogenesis is poorly understood. The Notch signaling pathway has been shown to be critically involved in tumorigenesis, including OS. Therefore, we explored the molecular mechanism by which the Notch-1 signaling pathway is involved in OS progression. Several approaches were carried out to determine the biological function of Notch-1 in OS cells. The MTT results revealed that Notch-1 overexpression increased the viability of OS cells, whereas Notch-1 downregulation reduced cell viability. Consistently, modulation of Notch-1 regulated apoptosis and the migratory and invasive abilities of OS cells. Mechanistic studies showed that Notch-1 overexpression augmented cell division cycle 20 (Cdc20) expression in OS cells. Moreover, overexpression of Cdc20 alleviated the inhibitory effects of Notch-1 downregulation on the viability, migration and invasion of OS cells. Our study offers a promising OS treatment strategy by inhibiting Notch-1.
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