Bone marrow fibroblasts induce expression of PI3K/NF-κB pathway genes and a pro-angiogenic phenotype in CLL cells
Bone marrow fibroblasts induce expression of PI3K/NF-κB pathway genes and a pro-angiogenic phenotype in CLL cells
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DOI：
10.1016/j.leukres.2008.03.003
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发表时间：
2008-10-01
影响因子：
2.7
通讯作者：
Duerig, J.
中科院分区：
文献类型：
--
作者：
Edelmann, J.;Klein-Hitpass, L.;Duerig, J.
使用基于微阵列的基因表达谱（GEP）来研究基质如何在采用鼠成纤维细胞系M2- 10 B4的体外共培养模型中调节CLL细胞的存活。与基质层（STR）直接接触培养的CLL细胞显示出比在M2- 10 B4细胞上方的transwell（TW）插入物中培养的细胞显著更好的存活。与TW条件相比，STR诱导了PI 3 K/NF-κ B促存活途径基因的显著上调，并通过上调血管内皮生长因子（VEGF）和骨桥蛋白（OPN）以及下调抗血管生成分子血小板反应蛋白-1（TSP-1）介导了CLL细胞中的促血管生成转换。(c)2008爱思唯尔有限公司保留所有权利。
Microarray-based gene expression profiling (GEP) was used to study how stroma modulates the survival of CLL cells in an in vitro coculture model employing the murine fibroblast cell line M2-10B4. CLL cells cultured in direct contact with the stromal layer (STR) showed a significantly better survival than cells cultured in transwell (TW) inserts above the M2-10B4 cells. STR as compared to TW conditions induced a significant up-regulation of PI3K/NF-kappa B pro-survival pathway genes and mediated a pro-angiogenetic switch in the CLL cells by up-regulation of vascular endothelial growth factor (VEGF) and osteopontin (OPN) and down-regulation of the anti-angiogenefic molecule thrombospondin-1 (TSP-1). (c) 2008 Elsevier Ltd. All rights reserved.