Regulation of in situ to invasive breast carcinoma transition
Regulation of in situ to invasive breast carcinoma transition
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DOI：
10.1016/j.ccr.2008.03.007
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发表时间：
2008-05-01
期刊：
影响因子：
50.3
通讯作者：
Polyak, Kornelia
中科院分区：
文献类型：
--
作者：
Hu, Min;Yao, Jun;Polyak, Kornelia
乳腺导管原位癌（DCIS）向浸润性癌的转变是乳腺肿瘤进展中的一个关键事件，目前尚不清楚。在这里，我们分析了肌上皮细胞和成纤维细胞在原位癌的进展中的作用，使用人类DCIS和原发性乳腺肿瘤的模型。成纤维细胞促进了侵袭的进展，而正常肌上皮细胞则抑制了侵袭的进展。分离的腔上皮细胞和肌上皮细胞的分子谱鉴定了涉及TGF β、Hedgehog、细胞粘附和肌上皮细胞分化所需的p63的复杂相互作用网络，其消除导致肌上皮细胞的损失和进展至侵袭。
The transition of ductal carcinoma in situ (DCIS) to invasive carcinoma is a poorly understood key event in breast tumor progression. Here, we analyzed the role of myoepithelial cells and fibroblasts in the progression of in situ carcinomas using a model of human DCIS and primary breast tumors. Progression to invasion was promoted by fibroblasts and inhibited by normal myoepithelial cells. Molecular profiles of isolated luminal epithelial and myoepithelial cells identified an intricate interaction network involving TGF beta, Hedgehog, cell adhesion, and p63 required for myoepithelial cell differentiation, the elimination of which resulted in loss of myoepithelial cells and progression to invasion.