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

Microcins are antimicrobial peptides (AMPs) with low molecular weight, which are produced by Enterobacterales and have broad-spectrum antibacterial activity. Alternative approaches like AMPs could help conventional anticancer treatments to fight malignant cells. The present study endeavors to examine the antitumor activity of microcins isolated from different Enterobacterales strains. 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. In addition, 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. 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. 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. The extract obtained from this isolate on the breast cancer cell line exhibited the most significant degree of toxicity after 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. Contrarily, it potentiated the reparative ability of nontumoral fibroblasts, supporting the in vitro safety toward normal cells and, at the same time, the selectivity against malignant ones. In summary, our results highlighted a significant growth suppression of breast cancer cells with an escalated rate of cellular demise via the apoptosis pathway.