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首页> 外文期刊>Journal of Cellular Physiology >Platelet-derived growth factor-B increases colon cancer cell growth in vivo by a paracrine effect.
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Platelet-derived growth factor-B increases colon cancer cell growth in vivo by a paracrine effect.

机译：血小板源生长因子b增加结肠癌体内癌细胞生长的旁分泌作用。

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PDGF-B released from colon tumor cells regulated tumor growth in athymic mice in a paracrine manner by inducing blood vessel formation. A positive correlation was found between expression of PDGF B-chain in cells grown in vitro and the number of factor VIII-positive blood vessels in tumors induced by three classes of colon carcinoma cell lines. Elevated expression of PDGF-B was also correlated with tumor size. Each cell line had the same mutations in the colon cancer genes APC, DCC, and p53 and had wild type c-K-ras genes (Huang et al. [1994] Oncogene, 9:3701-3706.) eliminating the possibility that any differences in tumor blood vessel formation were due to mutations and/or deletions in these genes. Colon carcinoma cells released biologically active PDGF capable of stimulating the growth of NIH3T3 cells, which was inhibited by neutralizing antisera to PDGF-AB chains. An inverse correlation was found between induction of factor VIII-positive blood vessels and expression of vascular endothelial growth factor (VEGF), while no correlation was seen with expression of either TGF alpha or k-FGF. Basic fibroblast growth factor (FGF) expression was not detected in these tumor cells. TGF beta 1 was capable of inducing PDGF-B expression in the undifferentiated U9 colon carcinoma cell line, but this sensitivity was not seen in differentiated cells. In contrast, TGF beta 1 inhibited VEGF expression in both undifferentiated cells and differentiated colon cancer cells. Thus, TGF beta 1 has two roles in the growth of undifferentiated U9 colon carcinoma cells in vivo: direct stimulation of cell proliferation as we have showed in earlier studies, and an increase in angiogenesis by inducing PDGF-B.
机译：PDGF-B从结肠肿瘤细胞释放监管小鼠肿瘤生长在无胸腺的旁分泌方式诱导血管形成。积极表达之间的相关性被发现的PDGF B-chain在体外和细胞生长VIII-positive血管数量的因素结肠肿瘤引起的三个类癌细胞系。PDGF-B也与肿瘤大小有关。结肠癌细胞系有相同的突变癌症基因APC, DCC、p53和野生型c-K-ras基因(黄等。[1994]致癌基因,9:3701 - 3706)消除的可能性肿瘤血管形成中的任何差异是由于突变和/或删除这些基因。生物活性PDGF刺激的能力NIH3T3细胞的生长,抑制通过中和抗血清PDGF-AB链。逆相关性被发现之间的感应VIII-positive血管和的因素血管内皮生长因子的表达(VEGF),而没有相关信息转化生长因子α或k-FGF的表情。纤维母细胞生长因子(FGF)表达式在这些肿瘤细胞检测。诱导PDGF-B表达的能力未分化U9结肠癌细胞系,但这敏感性未见的分化细胞。抑制VEGF表达未分化细胞和分化结肠癌细胞。未分化U9结肠癌癌的生长体内细胞:细胞的直接刺激正如我们前面已经显示增殖研究,增加血管生成诱导PDGF-B。

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