Department of Medicine I, Clinical Division of Oncology, Medical University of Vienna, A-1090 Vienna, Austria.
Mol Oncol. 2010 Apr;4(2):150-60. doi: 10.1016/j.molonc.2010.01.002. Epub 2010 Jan 7.
Cancer progression is often associated with the formation of malignant effusions. Vascular endothelial growth factor (VEGF) is a major regulator of vascular permeability and has been implicated as mediator of tumor progression. We examined the production and secretion of VEGF(165) in various primary cancer cells derived from malignant effusions, and the role of exogenous VEGF(165) as a mediator of effusion formation. VEGF(165) was constantly secreted by all cultured tumor cells in an mTOR-dependent manner, as it was inhibited by the mTOR inhibitor rapamycin. Secreted VEGF(165) showed functional activity by inducing endothelial leakiness and tumor cell-transendothelial migration in vitro, effects which could be reverted by the anti-VEGF antibody bevacizumab. Thus, mTOR inhibitors as well as bevacizumab should be considered as potential agents in cancer patients suffering from malignant effusions.
癌症的进展通常与恶性积液的形成有关。血管内皮生长因子（VEGF）是血管通透性的主要调节剂，被认为是肿瘤进展的介质。我们研究了源自恶性积液的各种原发性癌细胞中 VEGF（165）的产生和分泌，以及外源性 VEGF（165）作为积液形成的介质的作用。VEGF（165）以 mTOR 依赖的方式被所有培养的肿瘤细胞持续分泌，因为它被 mTOR 抑制剂 rapamycin 抑制。分泌的 VEGF（165）通过在体外诱导内皮通透性和肿瘤细胞穿过内皮迁移表现出功能活性，这些作用可以通过抗 VEGF 抗体 bevacizumab 逆转。因此，mTOR 抑制剂以及 bevacizumab 都应被视为患有恶性积液的癌症患者的潜在治疗药物。
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