微小RNA-184通过PI3K/AKT/mTOR增加癌症对顺铂的耐药性

IF 0.1 4区 医学
S. Ding, Keli Zhong, Kaibin Huang, Ligang Xia
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引用次数: 0

摘要

本研究旨在探讨miR-184在癌症(GC)细胞对顺铂(DDP)耐药性中的作用。因此,不仅BGC-823 DDP抗性GC细胞(BGC-823/DDP),而且SGC-7901 DDP抗性细胞(SGC-7901/DDP)与其亲本细胞相比都被上调。异位表达的miR-184模拟物增加了顺铂耐药性,增加了顺铂耐药细胞中的迁移和侵袭。尽管如此,miR-184抑制剂降低了DDP耐药性、细胞侵袭以及亲代细胞中的迁移。此外,Ncor2是GC细胞中miR-184的直接靶向基因。Ncor2基因敲除显示DDP抗性促进了顺铂抗性细胞。相反,在BGC-823细胞中过度表达Ncor2产生了抑制对顺铂耐药性的作用。此外,miR-184的过度表达提高了顺铂耐药细胞对DDP的耐药性,部分原因是Ncor2/PI3K/AKT/mTOR信号通路的激活。miR-184还可降低BGC-823/DDP细胞对顺铂的敏感性。总之,我们证明miR-184的失活或其靶基因通道的激活可以作为逆转GC中DDP耐药性的创新。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MicroRNA-184 Increases the Resistance of Gastric Cancer to Cisplatin via PI3K/AKT/mTOR
This study sought for investigating the function of miR-184 in resistance of gastric cancer (GC) cells to cisplatin (DDP). Consequently, not only BGC-823 DDP-resistant GC cells (BGC-823/DDP) but also SGC-7901 DDP-resistant cells (SGC-7901/DDP) were upregulated in contrast with their parent cells. Ectopic expressed miR-184 mimetics increased DDP resistance and increased migration as well as invasion in cisplatin-resistant cells. Nevertheless, miR-184 inhibitors reduced DDP resistance, cell invasion as well as migration in parent cells. Besides, Ncor2 is a direct targeting gene for miR-184 in GC cells. Ncor2 gene knockout revealed that DDP resistance promoted cisplatin-resistant cells. Conversely, over Ncor2 expression in BGC-823 cells generated the effect of suppressing resistance to cisplatin. Additionally, over miR-184 expression raised the resistance of cisplatin-resistant cells to DDP, in part arise from the activation of the Ncor2/PI3K/AKT/mTOR signal pathway. miR-184 could also lessen the sensitivity of BGC-823/DDP cells to cisplatin in vivo. To conclude, we evidence that the inactivation of miR-184 or the activation of channel of its target gene can be served as an innovation to reverse DDP resistance in GC.
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