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Gain in cellular organization of inflammatory breast cancer: A 3D in vitro model that mimics the in vivo metastasis

机译:在炎症性乳腺癌的细胞组织中获益:模拟体内转移的体外3D模型

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摘要

BackgroundThe initial step of metastasis in carcinomas, often referred to as the epithelial-mesenchymal transition (EMT), occurs via the loss of adherens junctions (e.g. cadherins) by the tumor embolus. This leads to a subsequent loss of cell polarity and cellular differentiation and organization, enabling cells of the embolus to become motile and invasive. However highly malignant inflammatory breast cancer (IBC) over-expresses E-cadherin. The human xenograft model of IBC (MARY-X), like IBC, displays the signature phenotype of an exaggerated degree of lymphovascular invasion (LVI) in situ by tumor emboli. An intact E-cadherin/α, β-catenin axis mediates the tight, compact clump of cells found both in vitro and in vivo as spheroids and tumor emboli, respectively.
机译:背景技术癌转移的初始步骤通常称为上皮-间质转化(EMT),是由于肿瘤栓子失去了粘附连接(例如钙黏着蛋白)而发生的。这导致随后细胞极性的丧失以及细胞分化和组织的丧失,使栓子的细胞变得运动和侵袭。但是,高度恶性的炎症性乳腺癌(IBC)过表达E-钙粘蛋白。与IBC一样,IBC(MARY-X)的人异种移植模型表现出肿瘤栓子在原位过大程度的淋巴管浸润(LVI)的特征表型。完整的E-cadherin /α,β-catenin轴介导在体外和体内分别以球状体和肿瘤栓子形式存在的紧密紧密的细胞团。

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