Comşa Şerban, Popescu Roxana, Avram Ştefana, Ceaușu Raluca Amalia, Cîmpean Anca Maria, Raica Marius
Department of Histology, Angiogenesis Research Center, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania.
Department of Cell and Molecular Biology, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania.
In Vivo. 2017 Mar-Apr;31(2):199-203. doi: 10.21873/invivo.11045.
To evaluate the interaction between MCF-7 breast cancer cells and the chick embryo chorioallantoic membrane (CAM) and the ability of bevacizumab to modulate this process.
We implanted MCF-7 cells onto CAM and repeatedly added bevacizumab to a subset of eggs. We then evaluated the morphological and immunohistochemical profiles of CAM and MCF-7.
MCF-7 cells entered the mesoderm and stimulated the mesenchymal cells to acquire vasculogenic and myofibroblastoid features. MCF-7 cells developed an estrogen receptor-, progesterone receptor-, p53- and Ki67-negative status and entered the epithelial-mesenchymal transition. Bevacizumab down-regulated the expression of B-cell lymphoma 2 protein (BCL-2), vascular endothelial growth factor (VEGF) and E-cadherin in MCF-7 and inhibited vasculogenesis.
MCF-7 cells turn the mesoderm of CAM into a surrogate tumor stroma. CAM induces a triple-negative, non-proliferative but still anti-apoptotic status in MCF-7 cells. Although antivasculogenic, bevacizumab stimulates MCF-7 cells to acquire a more aggressive status.
评估MCF-7乳腺癌细胞与鸡胚绒毛尿囊膜（CAM）之间的相互作用，以及贝伐单抗调节这一过程的能力。
我们将MCF-7细胞植入CAM，并对一部分鸡蛋反复添加贝伐单抗。然后，我们评估了CAM和MCF-7的形态学和免疫组织化学特征。
MCF-7细胞进入中胚层并刺激间充质细胞获得血管生成和成肌纤维样特征。MCF-7细胞呈现雌激素受体、孕激素受体、p53和Ki67阴性状态，并进入上皮-间质转化过程。贝伐单抗下调MCF-7中B细胞淋巴瘤2蛋白（BCL-2）、血管内皮生长因子（VEGF）和E-钙黏蛋白的表达，并抑制血管生成。
MCF-7细胞将CAM的中胚层转变为替代肿瘤基质。CAM诱导MCF-7细胞进入三阴性、非增殖但仍抗凋亡状态。尽管具有抗血管生成作用，但贝伐单抗刺激MCF-7细胞获得更具侵袭性的状态。
