Abstract
AIM: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.