Şerban Comşa1, Roxana Popescu2, Ştefana Avram1, Raluca Amalia Ceaușu1, Anca Maria Cîmpean3, Marius Raica1. 1. Department of Histology, Angiogenesis Research Center, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania. 2. Department of Cell and Molecular Biology, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania. 3. Department of Histology, Angiogenesis Research Center, Victor Babeş University of Medicine and Pharmacy, Timişoara, Romania ancacimpean1972@yahoo.com.
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. Copyright
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. Copyright
Authors: M Aonuma; Y Saeki; T Akimoto; Y Nakayama; C Hattori; Y Yoshitake; K Nishikawa; M Shibuya; N G Tanaka Journal: Int J Exp Pathol Date: 1999-10 Impact factor: 1.925
Authors: Euphemia Leung; Ji Eun Kim; Marjan Askarian-Amiri; Graeme J Finlay; Bruce C Baguley Journal: Biomed Res Int Date: 2014-03-04 Impact factor: 3.411