Wnt/β-catenin signaling pathway may regulate the expression of angiogenic growth factors in hepatocellular carcinoma.
Wnt/β-catenin signaling pathway may regulate the expression of angiogenic growth factors in hepatocellular carcinoma.
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DOI：
10.3892/ol.2014.1828
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发表时间：
2014-04
期刊：
影响因子：
2.9
通讯作者：
Wang XH
中科院分区：
文献类型：
--
作者：
Qu B;Liu BR;DU YJ;Chen J;Cheng YQ;Xu W;Wang XH
Wnt/β-catenin信号通路在肝细胞癌（HCC）的发生、发展过程中起着重要作用。本研究旨在探讨Wnt/β-catenin信号通路对HCC中血管生成生长因子表达的影响。用针对β-catenin的小干扰RNA（siRNA）转染HCC HepG 2细胞系。72 h和96 h后提取蛋白，Western blot检测β-catenin、基质金属蛋白酶（MMP）-2、MMP-9、血管内皮生长因子（VEGF）-A、VEGF-C和碱性成纤维细胞生长因子（bFGF）的表达水平。在两个时间点，β-连环蛋白蛋白表达均受到抑制。MMP-2、MMP-9、VEGF-A、VEGF-C和bFGF蛋白表达水平在转染后72 h下降，96 h上升。我们的研究结果表明，在肝癌细胞中，Wnt/β-catenin信号通路可能调节血管生成因子MMP-2、MMP-9、VEGF-A、VEGF-C和bFGF的蛋白表达。这些蛋白质是β-catenin信号的下游，也受其他因素的调节。结论：Wnt/β-catenin信号通路可能通过调控血管生成因子的表达，参与肝癌血管生成、浸润和转移的调控。
The Wnt/β-catenin signaling pathway plays a key role during hepatocellular carcinoma (HCC) genesis and development. The present study aimed to investigate the effects of the Wnt/β-catenin signaling pathway on the expression of angiogenic growth factors involved in HCC. The HCC HepG2 cell line was transfected with small interfering RNA (siRNA) against β-catenin. After 72 and 96 h, protein was extracted and the expression levels of β-catenin, matrix metalloproteinase (MMP)-2, MMP-9, vascular endothelial growth factor (VEGF)-A, VEGF-C and basic fibroblast growth factor (bFGF) were detected by western blot analysis. β-catenin protein expression was inhibited at both time points. Notably, MMP-2, MMP-9, VEGF-A, VEGF-C and bFGF protein expression levels decreased at 72 h and then increased at 96 h after transfection. Our results demonstrated that in HCC cells, the Wnt/β-catenin signaling pathway may regulate the protein expression of the angiogenic factors, MMP-2, MMP-9, VEGF-A, VEGF-C and bFGF. These proteins were downstream of β-catenin signaling and were also regulated by other factors. In conclusion, the Wnt/β-catenin signaling pathway may contribute to the regulation of HCC angiogenesis, infiltration and metastasis through regulating the expression of these angiogenic factors.
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