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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

VS-5584通过调节PI3K / mTOR和MAPK途径诱导G1期阻滞抑制人骨肉瘤细胞的生长

卷 20, 期 8, 2020

页: [616 - 623] 页: 8

弟呕挨: 10.2174/1568009620666200414150353

价格: $65

摘要

背景:PI3K / mTOR信号通路的激活在人类骨肉瘤的进展中起关键作用。 研究证实,VS-5584是PI3K / mTOR途径的新型抑制剂,并显示出潜在的抗癌活性。 目的:探讨VS-5584对人骨肉瘤细胞生长的抗癌作用及其潜在机制。 方法:培养U2OS和MG-63人骨肉瘤细胞,通过CCK8分析,流式细胞术和Western blot研究VS-5584处理细胞的细胞毒性,细胞凋亡。 细胞迁移和管形成也用于检查抗癌潜力。 结果:结果表明,VS-5584处理通过调节p21,p27,Cyclin B1和Cdc2诱导G1期阻滞,剂量依赖性地抑制U2OS和MG-63细胞的生长。 进一步的研究表明,VS-5584处理可有效抑制PI3K / mTOR信号通路并触发MAPK磷酸化。 此外,VS-5584处理可显着抑制HUVEC的细胞迁移和管形成,然后下调HIF-1α和VEGF。 结论:我们的发现证实了VS-5584可能是一种有前途的抗癌药物,在人骨肉瘤的化学疗法和化学预防中具有潜在的应用前景。

关键词: VS-5584,骨肉瘤,G1期阻滞,PI3K / mTOR,MAPK,细胞毒性。

图形摘要

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