Protective Effects of Antimicrobial Peptide Microcin J25 (MccJ25) Isolated from Escherichia coli against Breast Cancer Cells

Abstract

Introduction: Microcins are Antimicrobial peptides (AMPs) with low molecular weight, which are produced by Enterobacterales and have broad-spectrum antibacterial activity. They can selectively replace common cancer treatments in cancer cells with less side effects and higher effectiveness. Given the aforementioned context, the present study endeavors to examine the antitumor activity of microcins isolated from of the Enterobacterales. Material and Methods In total, 120 Enterobacterales isolates were examined after identification. Subsequently, the bacteria were subjected to an agar diffusion test to assess their antibacterial efficacy. Positive isolates were further examined for the presence of Mccj25 using PCR. The cytotoxic effects of isolates harboring the microcin gene were explored using quantitative real-time PCR (RT-qPCR) and the MTT test on breast cancer cells. Additionally, the expression levels of BCL2 and STAT3 genes were evaluated, and apoptosis was quantified using flow cytometry. The repair rate of normal cells was determined using a scratch assay. Results The findings obtained from the phenotypic and biochemical assays have duly verified and established the categorization of the Enterobacterales. After conducting the agar diffusion test, a total of 25 isolates of Escherichia coli and Klebsiella pneumoniae displaying inhibition zones were chosen as suitable specimens possessing AMPs. Urinary E. coli was identified as isolate 83. The analysis conducted on the expression of the Mccj25 gene within the aforementioned isolates indicated that isolate 83 exhibited significant expression of the Mccj25 gene. Conclusion The extract obtained from this isolate on the breast cancer cell line exhibited the most significant degree of toxicity after precisely 48 h. Furthermore, the treatment of breast cancer cells with isolate 83 showed that the rate of apoptosis was about 86%, and the expression of BCL2 and STAT3 genes decreased. Moreover, it potentiated the reparative ability of normal fibroblast cells. They resulted in growth suppression of breast cancer cells and elicited an escalated rate of cellular demise via the apoptosis pathway.