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首页> 外文期刊>Molecular and Cellular Endocrinology >PTHrP treatment of colon cancer cells promotes tumor associated-angiogenesis by the effect of VEGF
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PTHrP treatment of colon cancer cells promotes tumor associated-angiogenesis by the effect of VEGF

机译：通过VEGF的效果，结肠癌细胞的PTHRP治疗促进肿瘤相关血管生成

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摘要

We showed that Parathyroid Hormone-related Peptide (PTHrP) induces proliferation, migration, survival and chemoresistance via MAPKs and PI3K/AKT pathways in colorectal cancer (CRC) cells. The objective of this study was to investigate if PTHrP is also involved in tumor angiogenesis. PTHrP increased VEGF expression and the number of structures with characteristics of neoformed vessels in xenografts tumor. Also, PTHrP increased mRNA levels of VEGF, HIF-1 alpha and MMP-9 via ERK1/2 and PI3K/Akt pathways in Caco-2 and HCT116 cells. Tumor conditioned media (TCMs) from both cell lines treated with PTHrP increases the number of cells, the migration and the tube formation in the endothelial HMEC-1 cells, whereas the neutralizing antibody against VEGF diminished this response. In contrast, PTHrP by direct treatment only increased ERK1/2 phosphorylation and the HMEC-1 cells number. These results provide the first evidence related to the mode of action of PTHrP that leads to its proangiogenic effects in the CRC.
机译：我们表明，甲状旁腺激素相关的肽（PTHRP）通过映射（CRC）细胞的MAPK和PI3K / AKT途径诱导增殖，迁移，存活和化学态化。本研究的目的是调查PTHRP是否也参与肿瘤血管生成。 PTHRP增加了VEGF表达和卵黄移植物肿瘤中新型血管特性的结构数量。此外，PTHRP通过Caco-2和HCT116细胞中通过ERK1 / 2和PI3K / AKT途径增加了VEGF，HIF-1α和MMP-9的mRNA水平。用PTHRP处理的两条细胞系肿瘤条件培养基（TCMS）增加了内皮HMEC-1细胞中细胞的数量，迁移和管形成，而反对VEGF的中和抗体减少了这种反应。相比之下，通过直接治疗的PTHRP仅增加ERK1 / 2磷酸化和HMEC-1细胞数。这些结果提供了与PTHRP的作用方式相关的第一证据，导致其在CRC中的过致效应。

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