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首页> 外文期刊>The journal of clinical investigation >Cyclooxygenase-2–dependent lymphangiogenesis promotes nodal metastasisof postpartum breast cancer
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Cyclooxygenase-2–dependent lymphangiogenesis promotes nodal metastasisof postpartum breast cancer

机译：依赖环氧合酶2的淋巴管生成促进产后乳腺癌的淋巴结转移

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Breast involution following pregnancy has been implicated in the high rates of metastasisobserved in postpartum breast cancers; however, it is not clear how this remodelingprocess promotes metastasis. Here, we demonstrate that human postpartum breast cancershave increased peritumor lymphatic vessel density that correlates with increased frequencyof lymph node metastases. Moreover, lymphatic vessel density was increased in normalpostpartum breast tissue compared with tissue from nulliparous women. In rodents, mammarylymphangiogenesis was upregulated during weaning-induced mammary gland involution.Furthermore, breast cancer cells exposed to the involuting mammary microenvironmentacquired prolymphangiogenic properties that contributed to peritumor lymphatic expansion,tumor size, invasion, and distant metastases. Finally, in rodent models of postpartumbreast cancer, cyclooxygenase-2 (COX-2) inhibition during the involution window decreasednormal mammary gland lymphangiogenesis, mammary tumor-associated lymphangiogenesis, tumorcell invasion into lymphatics, and metastasis. Our data indicate that physiologicCOX-2–dependent lymphangiogenesis occurs in the postpartum mammary gland andsuggest that tumors within this mammary microenvironment acquire enhancedprolymphangiogenic activity. Further, our results suggest that the prolymphangiogenicmicroenvironment of the postpartum mammary gland has potential as a target to inhibitmetastasis and suggest that further study of the therapeutic efficacy of COX-2 inhibitorsin postpartum breast cancer is warranted.
机译：怀孕后的乳房退化涉及到产后乳腺癌的高转移率。然而，目前尚不清楚这种重塑过程如何促进转移。在这里，我们证明人类产后乳腺癌剃须增加了与淋巴结转移频率增加相关的癌周淋巴管密度。此外，与产后妇女的组织相比，正常的产后乳房组织的淋巴管密度增加了。在啮齿动物中，断奶诱导的乳腺对合过程中乳腺淋巴管生成被上调。此外，暴露于渐进的乳腺微环境中的乳腺癌细胞具有促淋巴管生成的特性，从而促进了周围淋巴扩张，肿瘤大小，侵袭和远处转移。最后，在产后乳腺癌的啮齿动物模型中，内旋窗期间对环氧合酶2（COX-2）的抑制作用会降低正常的乳腺淋巴管生成，乳腺肿瘤相关的淋巴管生成，肿瘤细胞浸入淋巴管和转移。我们的数据表明生理COX-2依赖的淋巴管生成发生在产后的乳腺中，并建议该乳腺微环境中的肿瘤获得增强的前淋巴管生成活性。此外，我们的结果表明，产后乳腺的前淋巴管生成微环境具有潜在的抑制转移的作用，并建议进一步研究COX-2抑制剂在产后乳腺癌中的治疗效果。

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