Hepcidin TH1-5 induces apoptosis and activate caspase-9 in MCF-7 cells

Saravanan, A Dharmaraj and Khamsah Suryati, Mohd and Mohammed Al-Kassim, Hassan (2016) Hepcidin TH1-5 induces apoptosis and activate caspase-9 in MCF-7 cells. Journal of Applied Pharmaceutical Science, 6 (2). 081-086. ISSN 22313354 [P]

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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.

Item Type: Article
Uncontrolled Keywords: Hepcidin TH1-5, apoptosis, caspase, intrinsic, MCF-7
Subjects: Q Science > QD Chemistry
Q Science > QH Natural history > QH301 Biology
Divisions: Faculty of Medicine
Depositing User: Syahmi Manaf
Date Deposited: 13 Sep 2022 05:04
Last Modified: 13 Sep 2022 05:04
URI: http://eprints.unisza.edu.my/id/eprint/7202

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