Research Article | Volume: 6, Issue: 2, February, 2016

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

Mohammed Al-kassim Hassana c Wan-Atirah Azeminb Saravanan Dharmaraja Khamsah Suryati Mohdb d   

Open Access   

Published:  Feb 27, 2016

DOI: 10.7324/JAPS.2016.60211

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-inducing effect of the cysteine-rich peptide in the present study. Annexin V-fluorescein isothiocyanate and propidium iodide (annexin V-FITC/PI) apoptosis assay was performed after treatment of the cells. In the determination of caspase activity and pathway of apoptosis, luminescent assay was also performed where caspase-3/7, caspase-8 and caspase-9 were evaluated. Results of annexin V-FITC/PI staining showed proportion of early apoptotic cell were 73.67 ± 4.93%, 61.00 ± 5.57% and 44.33 ± 2.52% at 24, 48 and 72 hours respectively, while late apoptotic cell were 6.33 ± 1.53%, 23 ± 3.56% and 34 ± 3.51% within the same time interval. Based on the data from the luminescence test, Hepcidin TH1-5 activated caspases-3/7 and -9 which suggests that the apoptosis induced was due to the peptide treatment. Hepcidin TH1-5 induced apoptosis in MCF-7 via the activation of caspase-9 of the intrinsic pathway. These results support our previous findings of the cytotoxicity of Hepcidin TH1-5 and indicate that the peptide may be a potential agent for breast cancer therapy.

Keyword:     Hepcidin TH1-5 apoptosis caspase intrinsic MCF-7.


Hassan MA, Azemin W, Dharmaraj S, Mohd KS. Hepcidin Th1-5 Induces Apoptosis and Activate Caspase-9 in Mcf-7 Cells. J App Pharm Sci, 2016; 6 (02): 081-086.

Copyright:The Author(s). This is an open access article distributed under the Creative Commons Attribution Non-Commercial License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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