TY - JOUR ID - 251743 TI - Melittin Prevents Metastasis Of Epidermal Growth Factor-Induced MDA-MB-231 Cells Through The Inhibition Of The SDF-1α/CXCR4 Signaling Pathway JO - Cell Journal (Yakhteh) JA - CELLJ LA - en SN - 2228-5806 AU - Salimian, Fatemeh AU - Nabiuni, Mohammad AU - Salehghamar, Ensieh AD - Department of Cell and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran AD - 4Department of Cell and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran Y1 - 2022 PY - 2022 VL - 24 IS - 2 SP - 85 EP - 90 KW - CXCR4 KW - Melittin KW - Rac1 KW - SDF-1α DO - 10.22074/cellj.2022.7626 N2 - Objective: Melittin is one of the natural components of bee venom (Apis mellifera), and its anticancer and antimetastaticproperties have been well established, but the underlying mechanism remains elusive. The MDA-MB-231 is a triplenegative cell line that is highly aggressive and invasive. Besides, many critical proteins are involved in tumor invasion and metastasis. In this study, we investigated whether melittin inhibits the migration and metastasis of epidermal growth factor (EGF)-induced MDA-MB-231 cells via the suppression of SDF-1α/CXCR4 and Rac1-mediated signaling pathways.Materials and Methods: In this experimental study, cells were treated with melittin (0.5-4 μg/ml), and the toxicity of melittin was assessed by the MTT assay. Afterward, the migration assay was conducted to measure the degree of the migration of EGF-induced cells. The western blot technique was performed to analyze the rate of Rac1, p-Rac1, SDF1α, and CXCR4 expression in different groups.Results: The results demonstrated that melittin markedly suppressed the migration of EGF-induced cells and decreasedthe expression of p-Rac1, CXCR4, and SDF-1α proteins.Conclusion: The results of the present study suggested that the anti-tumor properties of melittin could be through theblocking of the SDF-1α/CXCR4 signaling pathway, which is beneficial for the reduction of tumor migration and invasion. UR - https://www.celljournal.org/article_251743.html L1 - https://www.celljournal.org/article_251743_874495d443b502f7f0303d1f4b115a5f.pdf ER -