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کلیدواژهها
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Breast cancer, Antimicrobial peptide, Apoptosis, Tilapia piscidin 4, ROS; DNA damage
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چکیده
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Antimicrobial peptides (AMPs), including Tilapia piscidin 4 (TP4), have emerged as a promising
therapeutic approach for treating different types of cancers. These peptides specifically target tumor
cells while minimizing harm to normal tissues. This study aims to investigate the cytotoxic effects of
TP4 and elucidate its molecular mechanisms of apoptosis in MCF-7 human breast cancer cell line. MCF-
7 and MCF-10 cell viability was assessed after treating the cells with various concentrations of TP4 for
24 h using the MTT assay. The MCF-7 cells were allocated into three groups including control cells (Cnt),
cells treated with 0.5 IC50, and 0.25 IC50 of TP4. The results demonstrated the inhibitory effect of TP4
on MCF-7 cell proliferation after 24 h (IC50 = 50.11 μg/mL), while no cytotoxicity was observed in normal
breast cells (MCF-10) at this concentration. The selectivity index (SI) value exceeded 2, indicating
TP4’s high specificity for cancer cells. Treatment with 25% and 50% IC50TP4 induced apoptosis, DNA
fragmentation, and mitochondrial membrane potential changes (JC-1 staining) in MCF-7 cells. This
induction was accompanied by increased expression of apoptotic genes (Bax, caspase3, and p53),
decreased expression of the anti-apoptotic gene Bcl2, elevated levels of intracellular reactive oxygen
species (ROS) and malondialdehyde (MDA) content, and reduced activity of the superoxide dismutase
(SOD) and catalase (CAT) enzymes when compared to the control group (P < 0.05). Based on the data,
we can infer that TP4 induces apoptosis in breast cancer cells via a ROS-dependent pathway.
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