miR-145 promoted anoikis resistance in tumor endothelial cells.
miR-145 promoted anoikis resistance in tumor endothelial cells.
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DOI：
10.1093/jb/mvx033
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发表时间：
2017-08
影响因子：
2.7
通讯作者：
K. Hida;T. Kawamoto;N. Maishi;M. Morimoto;Kosuke Akiyama;N. Ohga;M. Shindoh;N. Shinohara;Y. Hida
中科院分区：
文献类型：
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作者：
K. Hida;T. Kawamoto;N. Maishi;M. Morimoto;Kosuke Akiyama;N. Ohga;M. Shindoh;N. Shinohara;Y. Hida
肿瘤进展依赖于肿瘤血管生成。我们先前报道肿瘤内皮细胞（TEC）的表型不同于正常内皮细胞（NECs）。在此，我们使用公共TEC微阵列数据库进行了通路分析，并鉴定了几种推定的TEC特异性miRNA。我们发现miR-145在TEC中表达上调，miR-145增强了细胞粘附和抗失巢凋亡，并通过ERK 1/2上调了人微血管内皮细胞中的Bcl-2和Bcl-xl。这些发现表明miR-145部分参与TEC表型的获得。因此，miR-145及其靶基因可能成为抗血管生成治疗的分子靶点。
Tumor progression is dependent on tumor angiogenesis. We previously reported that the phenotype of tumor endothelial cells (TECs) is distinct from normal endothelial cells (NECs). Herein, we conducted a pathway analysis using a public TEC microarray database and identified several putative TEC-specific miRNAs. We found that miR-145 expression was upregulated in TECs and that miR-145 enhanced cell adhesion and anoikis resistance and upregulated Bcl-2 and Bcl-xl via ERK1/2 in human microvascular endothelial cells. These findings suggested that miR-145 is involved in the acquisition of the TEC phenotype, partially. Therefore, miR-145 and its target genes may be molecular targets for anti-angiogenic therapy.