Abstract

Objective: Melittin is one of the natural components of bee venom (Apis mellifera), and its anticancer and antimetastatic properties 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 decreased the 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 the blocking of the SDF-1α/CXCR4 signaling pathway, which is beneficial for the reduction of tumor migration and invasion.

Details

Title
Melittin Prevents Metastasis Of Epidermal Growth Factor-Induced MDA-MB-231 Cells Through The Inhibition Of The SDF-1α/CXCR4 Signaling Pathway
Author
Salimian, Fatemeh; Nabiuni, Mohammad; Salehghamar, Ensieh
Pages
85-90
Section
Original Article
Publication year
2022
Publication date
2022
Publisher
Royan Institute of Iran
ISSN
22285806
e-ISSN
22285814
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2830861663
Copyright
© 2022. This work is published under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.