Research Article

RPS24c亚型通过促进MVIH在结直肠癌中的稳定性促进肿瘤血管生成

卷 20, 期 5, 2020

页: [388 - 395] 页: 8

弟呕挨: 10.2174/1566524019666191203123943

价格: $65

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摘要

背景:结直肠癌(CRC)是全球第二大死亡原因,远处转移是晚期CRC患者预后不良的原因。 RPS24(核糖体蛋白S24)作为核糖体蛋白,已发现该基因编码不同同工型的多个转录变体。我们以前的研究表明,RPS24在CRC中过表达。但是,尚未完全确定RPS24在肿瘤发生中的作用机理。 方法:采用实时荧光定量PCR或western blotting定量检测CRC组织和细胞株RPS24亚型和lncRNA MVIH的表达。进行内皮管形成测定以确定RPS24对肿瘤血管生成的作用。通过MTT法测定HUVEC的细胞活力,并通过transwell法检测HUVEC的迁移和侵袭能力。用特异性ELISA试剂盒测试了PGK1的分泌。 结果:在这里,我们发现RPS24c亚型是肿瘤血管生成的主要贡献者,这是肿瘤生长和转移的重要过程。实时PCR显示,RPS24c同工型在CRC组织中高表达,而其他同工型在正常和CRC组织中均存在,无统计学差异。而且RPS24蛋白水平的变化主要是由于RPS24c的波动所致。此外,我们观察到,沉默RPS24c可以通过抑制小管形成,HUVEC细胞增殖和迁移来减少血管生成。此外,我们调查了分子机制,并证明RPS24c mRNA与lncRNA MVIH相互作用,结合相互作用增强了彼此的稳定性,从而通过抑制PGK1的分泌而激活了血管生成。 结论:RPS24c通过RPS24c / MVIH / PGK1途径促进CRC中的肿瘤血管生成。 RPS24c抑制可能是CRC中抗血管治疗的新选择。

关键词: RPS24,同工型,结直肠癌,血管生成,MVIH,PGK1。

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