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首页> 外文期刊>Cancer Cell >Regulation of tumor angiogenesis by integrin-linked kinase (ILK).
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Regulation of tumor angiogenesis by integrin-linked kinase (ILK).

机译:整联蛋白连接激酶(ILK)调节肿瘤血管生成。

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摘要

We show that integrin-linked kinase (ILK) stimulates the expression of VEGF by stimulating HIF-1alpha protein expression in a PKB/Akt- and mTOR/FRAP-dependent manner. In human prostate cancer cells, knockdown of ILK expression with siRNA, or inhibition of ILK activity, results in significant inhibition of HIF-1alpha and VEGF expression. In endothelial cells, VEGF stimulates ILK activity, and inhibition of ILK expression or activity results in the inhibition of VEGF-mediated endothelial cell migration, capillary formation in vitro, and angiogenesis in vivo. Inhibition of ILK activity also inhibits prostate tumor angiogenesis and suppresses tumor growth. These data demonstrate an important and essential role of ILK in two key aspects of tumor angiogenesis: VEGF expression by tumor cells and VEGF-stimulated blood vessel formation.
机译:我们显示整联蛋白连接激酶(ILK)通过以PKB / Akt-和mTOR / FRAP依赖性方式刺激HIF-1alpha蛋白表达来刺激VEGF的表达。在人类前列腺癌细胞中,用siRNA抑制ILK表达或抑制ILK活性会导致HIF-1alpha和VEGF表达的显着抑制。在内皮细胞中,VEGF刺激ILK活性,抑制ILK表达或活性可抑制VEGF介导的内皮细胞迁移,体外毛细血管形成和体内血管生成。 ILK活性的抑制还抑制前列腺肿瘤血管生成并抑制肿瘤生长。这些数据证明了ILK在肿瘤血管生成的两个关键方面的重要作用:肿瘤细胞的VEGF表达和VEGF刺激的血管形成。

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