【文摘发布】NATURE MEDICINE 的好文章－压力可促进
Cancer despite immunosurveillance: immunoselection and immunosubversionChronic stress promotes tumor growth and angiogenesisin a mouse model of ovarian carcinomaStress can alter immunological, neurochemical andendocrinological functions, but its role in cancer progressionis not well understood. Here, we show that chronic behavioralstress results in higher levels of tissue catecholamines, greatertumor burden and more invasive growth of ovarian carcinomacells in an orthotopic mouse model. These effects are mediatedprimarily through activation of the tumor cell cyclic AMP(cAMP)–protein kinase A (PKA) signaling pathway by the b2adrenergic receptor (encoded by ADRB2). Tumors in stressedanimals showed markedly increased vascularization andenhanced expression of VEGF, MMP2 and MMP9, and wefound that angiogenic processes mediated the effects of stresson tumor growth in vivo. These data identify b-adrenergicactivation of the cAMP–PKA signaling pathway as a majormechanism by which behavioral stress can enhance tumorangiogenesis in vivo and thereby promote malignant cell growth. These data also suggest that blocking ADRB-mediatedangiogenesis could have therapeutic implications for themanagement of ovarian cancer.
我们已知紧张状态可以改变生物体免疫、神经内分泌功能，但是在肿瘤发生、发展过程中的作用还不是很明确。本研究显示了慢性压力可以导致小鼠卵巢癌模型产生高水平的儿茶酚胺、使肿瘤瘤负荷增加和浸润性生长。最初是b2 肾上腺素受体（ 由ADRB2编码）通过激活肿瘤细胞CAMP-PKA信号通路所导致，处于紧张状态的动物血管生成和VEGF MMP2 MMP9表达明显增强，同时我们发现在活体细胞中，紧张状态介导的血管生成可促进肿瘤生长，这些数据进一步证实了CAMP-PKA信号通路的b 肾上腺素的激活是慢性压力在活体动物中促进肿瘤血管生成和肿瘤生长的主要机制。因此阻止ADRB介导的血管生长有可能作为治疗卵巢癌一种手段。
Nature Reviews Immunology 6, 715-727 (October 2006) | doi:10.1038/nri1936
http://www.nature.com/nri/journal/v6/n10/full/nri1936.html
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作者:admin@医学,生命科学 2011-03-25 05:15
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