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首页> 外文期刊>The Journal of Clinical Investigation: The Official Journal of the American Society for Clinical Investigation >Cyclooxygenase-2-dependent lymphangiogenesis promotes nodal metastasis of postpartum breast cancer
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Cyclooxygenase-2-dependent lymphangiogenesis promotes nodal metastasis of postpartum breast cancer

机译：环氧合酶-2依赖性淋巴管生成促进产后乳腺癌淋巴结转移

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摘要

Breast involution following pregnancy has been implicated in the high rates of metastasis observed in postpartum breast cancers; however, it is not clear how this remodeling process promotes metastasis. Here, we demonstrate that human postpartum breast cancers have increased peritumor lymphatic vessel density that correlates with increased frequency of lymph node metastases. Moreover, lymphatic vessel density was increased in normal postpartum breast tissue compared with tissue from nulliparous women. In rodents, mammary lymphangiogenesis was upregulated during weaning-induced mammary gland involution. Furthermore, breast cancer cells exposed to the involuting mammary microenvironment acquired prolymphangiogenic properties that contributed to peritumor lymphatic expansion, tumor size, invasion, and distant metastases. Finally, in rodent models of postpartum breast cancer, cyclooxygenase-2 (COX-2) inhibition during the involution window decreased normal mammary gland lymphangiogenesis, mammary tumor-associated lymphangiogenesis, tumor cell invasion into lymphatics, and metastasis. Our data indicate that physiologic COX-2-dependent lymphangiogenesis occurs in the postpartum mammary gland and suggest that tumors within this mammary microenvironment acquire enhanced prolymphangiogenic activity. Further, our results suggest that the prolymphangiogenic microenvironment of the postpartum mammary gland has potential as a target to inhibit metastasis and suggest that further study of the therapeutic efficacy of COX-2 inhibitors in postpartum breast cancer is warranted.
机译：妊娠后乳房退化与产后乳腺癌的高转移率有关;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的肿瘤周围淋巴管密度增加，这与淋巴结转移频率的增加有关。此外，与未产妇组织相比，正常产后乳腺组织的淋巴管密度增加。在啮齿动物中，乳腺淋巴管生成在断奶诱导的乳腺退化期间上调。此外，暴露于消退乳腺微环境的乳腺癌细胞获得了促淋巴管生成特性，有助于肿瘤周围淋巴扩张、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，环氧合酶-2（COX-2）抑制在退化窗口期间减少了正常的乳腺淋巴管生成、乳腺肿瘤相关淋巴管生成、肿瘤细胞侵入淋巴管和转移。我们的数据表明，生理性 COX-2 依赖性淋巴管生成发生在产后乳腺中，并表明该乳腺微环境中的肿瘤获得了增强的促淋巴管生成活性。此外，我们的研究结果表明，产后乳腺的促淋巴管生成微环境具有抑制转移的潜力，并表明有必要进一步研究 COX-2 抑制剂在产后乳腺癌中的治疗效果。

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