2月14日，澳大利亚研究人员称，阿司匹林等非甾体抗炎症药物或许能够抑制癌细胞扩散，原因是它们有助于切断输送这类细胞的“高速公路”。
长期以来，研究人员推测，阿司匹林等非甾体抗炎药可帮助抑制恶性肿瘤扩散，却没有能在药理层面解释作用机理。
墨尔本彼得·麦卡勒姆癌症研究中心研究人员14日说，“阿司匹林这类药物的分子……能有效抑制淋巴管扩张，从而削弱肿瘤扩散至身体其他部位的能力”。
在由美国《癌细胞》杂志发表的论文中，研究人员解释，肿瘤细胞扩散时，淋巴管内细胞中一种特定基因改变“表达”，成为肿瘤生长和细胞输送的连接点，可能引发全身淋巴管炎症和扩张。淋巴管一旦扩张，肿瘤细胞经由它扩散的能力随之增强。
阿司匹林可以抑制淋巴管的扩张，达到切断肿瘤细胞输送通道的效果。
研究人员史蒂芬·施特克尔说：“这就好比，我们找到了所有助推（癌细胞扩散）因素之间的关键连接点。”
研究人员预测，这项发现可用来研发新药，遏制乳腺癌、前列腺癌等实体恶性肿瘤的扩散，也可用于在肿瘤细胞扩散前发出“预警”。(生物谷 Bioon.com)
doi:10.1016/j.ccr.2011.12.026
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VEGF-D Promotes Tumor Metastasis by Regulating Prostaglandins Produced by the Collecting Lymphatic Endothelium
Tara Karnezis, Ramin Shayan, Carol Caesar, Sally Roufail, Nicole C. Harris, Kathryn Ardipradja, You Fang Zhang, Steven P. Williams, Rae H. Farnsworth, Ming G. Chai, Thusitha W.T. Rupasinghe, Dedreia L. Tull, Megan E. Baldwin, Erica K. Sloan, Stephen B. Fox, Marc G. Achen, Steven A. Stacker
Lymphatic metastasis is facilitated by lymphangiogenic growth factors VEGF-C and VEGF-D that are secreted by some primary tumors. We identified regulation of PGDH, the key enzyme in prostaglandin catabolism, in endothelial cells of collecting lymphatics, as a key molecular change during VEGF-D-driven tumor spread. The VEGF-D-dependent regulation of the prostaglandin pathway was supported by the finding that collecting lymphatic vessel dilation and subsequent metastasis were affected by nonsteroidal anti-inflammatory drugs (NSAIDs), known inhibitors of prostaglandin synthesis. Our data suggest a control point for cancer metastasis within the collecting lymphatic endothelium, which links VEGF-D/VEGFR-2/VEGFR-3 and the prostaglandin pathways. Collecting lymphatics therefore play an active and important role in metastasis and may provide a therapeutic target to restrict tumor spread.
