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首页> 外文期刊>International Journal of Clinical and Experimental Pathology >KRT6 interacting with notch1 contributes to progression of renal cell carcinoma, and aliskiren inhibits renal carcinoma cell lines proliferation in vitro
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KRT6 interacting with notch1 contributes to progression of renal cell carcinoma, and aliskiren inhibits renal carcinoma cell lines proliferation in vitro

机译:KRT6与notch1相互作用促进肾细胞癌的进展,而阿利吉仑在体外抑制肾癌细胞的增殖

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摘要

Notch signaling is a conserved and widely expressed signaling pathway, which mediates various physiological processes including tumorigenesis. This study aims to explore the potential role and mechanism of notch1 interacting with KRT6B in the progression of RCC. The results indicated that the mRNA and protein expression of notch1 and KRT6 were significantly increased in tumor tissues, and highly positive correlation existed between notch1 and KRT6. Moreover, the patients with high notch1 expression had a significantly poorer prognosis than those of low expression patients. In vitro, KRT6 loss-of-function could inhibit the expression of notch1 and induce renal carcinoma cell death. Eventually, we found that renin inhibitor, aliskiren, could inhibit cell proliferation and decrease the expression of notch1 and KRT6 as well as regulate apoptosis-related protein expression in 786-O and ACHN renal carcinoma cell lines. These results suggested that the upregulation of notch1 and KRT6B might be involved in the development, progression and prognosis of human RCC, and aliskiren could suppress renal carcinoma cell proliferation, at least partially, through downregulation the expression of notch1 and KRT6.
机译:Notch信号传导是一种保守且广泛表达的信号传导途径,其介导包括肿瘤发生在内的各种生理过程。本研究旨在探讨Notch1与KRT6B相互作用在RCC进展中的潜在作用和机制。结果表明,Notch1和KRT6的mRNA和蛋白表达在肿瘤组织中显着增加,并且Notch1和KRT6之间存在高度正相关。此外,notch1表达高的患者的预后明显低于低表达的患者。在体外,KRT6功能丧失可抑制notch1的表达并诱导肾癌细胞死亡。最终,我们发现肾素抑制剂阿利吉仑可以抑制786-O和ACHN肾癌细胞系中的细胞增殖并降低notch1和KRT6的表达,并调节凋亡相关蛋白的表达。这些结果表明,notch1和KRT6B的上调可能参与了人类RCC的发生,发展和预后,而阿利吉仑可以通过下调notch1和KRT6的表达至少部分地抑制肾癌细胞的增殖。

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