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  • br Statistical analysis br Data are presented

    2020-08-18


    4.11. Statistical analysis
    Data are presented as mean ± standard deviation. SPSS 16.0 (SPSS, Chicago, IL) software was applied to perform statistical analysis.
    Competing interests
    The authors declare that they have no competing interests.
    Acknowledgements
    This research was supported by grants from Sichuan Provincial Department of Science and Technology key research and development projects (No. 2018ZX09201018-029), National Natural Science Foundation of China youth science foundation project (No. 81703820).
    Author contributions
    Conceived and designed the experiments: J.N. Zhao. Performed the
    experiments: A.Q. Zeng. Analyzed the data: H. Hua, L. Liu. Wrote the
    Appendix A. Supplementary data
    References
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    Contents lists available at ScienceDirect
    Cellular Signalling
    journal homepage: www.elsevier.com/locate/cellsig
    Bevacizumab induces inflammation in MDA-MB-231 breast cancer cell line T and in a mouse model
    Layal EL-Hajjara,1, Nour Jalaleddinea,1, Abdullah Shaitob, Kazem Zibarac, Jalal M. Kazand,2, Jamal El-Saghird, Marwan El-Sabband,
    a Department of Biological and Environmental Sciences, Faculty of Science, Beirut Arab University, Beirut, Lebanon
    b Department of Biological and Chemical Sciences, Faculty of Arts and Sciences, Lebanese International University, Beirut, Lebanon
    c ER045– Laboratory of Stem Cells, PRASE, Biology Department, Faculty of Sciences, Lebanese University, Beirut, Lebanon
    d Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
    Keywords: Inflammation
    Angiogenesis NF-κB
    Connexin 43
    Breast cancer
    Metastasis 
    Background: Bevacizumab or Avastin® (Av) is an anti-vascular endothelial growth factor agent. It does not im-prove survival of breast cancer patients due to development of refractoriness. Av treatment was shown to in-crease inflammation in a diabetic mouse model, and also to induce epithelial-to-mesenchymal transition of non-transformed breast epithelia. This study aimed to understand if the Av-induced inflammatory microenvironment could be a mechanism of Av refractoriness. Expression profiles of inflammatory mediators, in vitro in MDA-MB-231 cells, in vivo in a mouse model xenografted with MDA-MB-231 cells and from archived cases of human breast carcinoma tissues were evaluated. Gap junctions are also crucial for angiogenesis and tumor cell extravasation. The effect of connexin 43 (Cx43) overexpression on the expression of inflammatory markers in MDA-MB-231 cells treated with Av was assessed.