Hepcidin TH1-5 Induces Apoptosis and Activate Caspase-9 in MCF-7 Cells

2016-03-02T05-40-04Z
Source: Journal of Applied Pharmaceutical Science
Mohammed Al-kassim Hassan, Wan-Atirah Azemin, Saravanan Dharmaraj, Khamsah Suryati Mohd.
Breast cancer is the most commonly diagnosed and leading cause of cancer deaths among women globally. In continuation of our investigation into the cytotoxicity of the antimicrobial peptide, hepcidin TH1-5, on human breast adenocarcinoma cell line (MCF-7), we further affirm the apoptosis induction effect of the cysteine-rich antimicrobial peptide in the present study. Annexin V-fluorescein isothiocyanate and propidium iodide (annexin V-FITC/PI) apoptosis assay was carried out after treatment of the cells. In the determination of caspase activity and pathway of apoptosis, luminescence assay was also performed where caspase-3/7, caspase-8 and caspase-9 were evaluated at time 12, 24 and 48 hours. Results of annexin V-FITC/PI staining showed that 44.33%, 34.33%, 9.67% of the cell were in the early apoptosis, late apoptosis and necrotic stages respectively after 72 hours of treatment. Based on the data from the luminescence test, hepcidin TH1-5 activates caspases-3/7 and -9 which suggests that the apoptosis induced may be due to the peptide treatment. Hepcidin TH1-5 may have induced apoptosis in MCF-7 cells via the activation of caspase-9 of the intrinsic pathway. These results support our previous findings of the cytotoxicity of hepcidin TH1-5 and indicated that the peptide may be a potential agent for breast cancer therapy.


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