Department of Bio and Brain Engineering, KAIST, Daejeon 305-701, Republic of Korea.
Cancer Lett. 2011 Oct 28;309(2):145-50. doi: 10.1016/j.canlet.2011.05.026. Epub 2011 Jun 16.
Analysis using the public microarray database Gene Expression Omnibus indicates significantly higher mRNA expression of VEGF and VEGFRs in colorectal cancer and high grade astrocytoma but not in hepatocellular carcinoma compared to normal tissue. Human malignant astrocytoma cell lines (U251-MG and U373-MG) and HT-1080 fibrosarcoma cells expressed relatively higher levels of VEGF and VEGFRs compared to hepatocellular and colorectal cancer cell lines. Administration of exogenous VEGF-A induced cell growth in a dose-dependent fashion in astrocytoma and fibrosarcoma cells but not in colorectal and hepatocellular cancer cells. The blockade of VEGF inhibited cell survival only in U251-MG, U373-MG and HT-1080 cells. These results collectively suggest the role of autocrine VEGF signaling in various cancer cells and provide a basis for the variable clinical responses to antiangiogenic therapy observed in different types of malignancies.
利用公共基因表达数据库 Gene Expression Omnibus 进行分析表明，与正常组织相比，结直肠癌和高级别星形细胞瘤中 VEGF 和 VEGFRs 的 mRNA 表达水平显著升高，但肝癌中则不然。人类恶性星形细胞瘤细胞系（U251-MG 和 U373-MG）和 HT-1080 纤维肉瘤细胞表达的 VEGF 和 VEGFRs 水平相对高于肝癌和结直肠癌细胞系。外源性 VEGF-A 的给药以剂量依赖的方式诱导星形细胞瘤和纤维肉瘤细胞的细胞生长，但不诱导结直肠和肝癌细胞的细胞生长。VEGF 的阻断仅抑制 U251-MG、U373-MG 和 HT-1080 细胞的存活。这些结果共同表明自分泌 VEGF 信号在各种癌细胞中的作用，并为不同类型恶性肿瘤中观察到的抗血管生成治疗的可变临床反应提供了依据。
