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1860799433213476864
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INTELEK Repository
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Online Access
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https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072
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| date |
2015-06-24 09:33:37
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| eventvenue |
Johor Bahru, Malaysia
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Restricted Document
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5986
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UniSZA
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0718-01-FH03-FBIM-15-03281.pdf
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| person |
Hadi Nur
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| recordtype |
oai_dc
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https://intelek.unisza.edu.my/intelek/pages/view.php?ref=5986
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5986 https://intelek.unisza.edu.my/intelek/pages/view.php?ref=5986 https://intelek.unisza.edu.my/intelek/pages/search.php?search=!collection407072 Restricted Document Conference Conference Paper application/pdf 6 1.6 Adobe Acrobat Pro DC 20 Paper Capture Plug-in Hadi Nur 2015-06-24 09:33:37 0718-01-FH03-FBIM-15-03281.pdf UniSZA Private Access Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5 Antimicrobial peptides (AMPs) have been reported to display multifunctional properties as potential therapeutic agents. They exhibit rapid killing and a broad spectrum of activity against Gram-positive and Gram-negative bacteria, fungi, parasites, enveloped viruses and tumour cells. An AMP, hepcidin TH1-5 (HepTH1-5) is a small and cationic peptide was shown as important innate immune defense in Tilapia (Oreochromis mossambicus). Recent studies have shown that synthetically derived HepTH1-5 displayed cytotoxic effect on tested cancer cell lines. In this study, we aimed to investigate the cytotoxic and apoptosis effects of HepTH1-5 on HL-60, HepG2 and HeLa cells and compare to noncancerous cell lines, Chang and NIH/3T3. We also investigated the effect of this peptide on cell cycle. Cytotoxic assay by MTT revealed that HepTH1-5 is highly cytotoxic on HepG2, HeLa and HL-60 cells with IC50 of 8.58 x10-4 µM, 0.011 µM and 0.0858 µM respectively. These results also comparable with methotrexate, a standard chemotherapy drug. Intriguingly, it does not show significant cytotoxicity against normal cells. Apoptogenic effects of HepTH1-5 were studied by acridine orange/propidium iodide staining and revealed that after 24h treatment, 61.2% of HepG2 cells were in early apoptosis, 20.7% in late apoptosis while 1% of cells were in necrosis. In contrast, after 24h treatment with methotrexate, only 18.2% of cells were in early apoptosis, whereas 76.3% were in late apoptosis. This trend was continued after 48h treatment but prolonged incubation of 72h saw a dramatic change in the apoptotic effect where less than 12% of cells were at early apoptosis while more than 79.7% were at late apoptosis. Cell cycle analysis on HepG2 cells showed that HepTH1-5 was able to block cell at G2/M phase significantly but not in HeLa while methotrexate arrest cells at G0/G1 phase. This data revealed that apoptosis effect of HepTH1-5 and methotrexate in cell cycle might occur at different mechanism. Taking all the data together, it was found that HepTH1-5 significantly triggers apoptosis in cancerous cells and it shows that this peptide could potentially be developed as anticancer agent. International Conference on Natural Product 2015 Johor Bahru, Malaysia
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| spellingShingle |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| summary |
Antimicrobial peptides (AMPs) have been reported to display multifunctional properties as potential therapeutic agents. They exhibit rapid killing and a broad spectrum of activity against Gram-positive and Gram-negative bacteria, fungi, parasites, enveloped viruses and tumour cells. An AMP, hepcidin TH1-5 (HepTH1-5) is a small and cationic peptide was shown as important innate immune defense in Tilapia (Oreochromis mossambicus). Recent studies have shown that synthetically derived HepTH1-5 displayed cytotoxic effect on tested cancer cell lines. In this study, we aimed to investigate the cytotoxic and apoptosis effects of HepTH1-5 on HL-60, HepG2 and HeLa cells and compare to noncancerous cell lines, Chang and NIH/3T3. We also investigated the effect of this peptide on cell cycle. Cytotoxic assay by MTT revealed that HepTH1-5 is highly cytotoxic on HepG2, HeLa and HL-60 cells with IC50 of 8.58 x10-4 µM, 0.011 µM and 0.0858 µM respectively. These results also comparable with methotrexate, a standard chemotherapy drug. Intriguingly, it does not show significant cytotoxicity against normal cells. Apoptogenic effects of HepTH1-5 were studied by acridine orange/propidium iodide staining and revealed that after 24h treatment, 61.2% of HepG2 cells were in early apoptosis, 20.7% in late apoptosis while 1% of cells were in necrosis. In contrast, after 24h treatment with methotrexate, only 18.2% of cells were in early apoptosis, whereas 76.3% were in late apoptosis. This trend was continued after 48h treatment but prolonged incubation of 72h saw a dramatic change in the apoptotic effect where less than 12% of cells were at early apoptosis while more than 79.7% were at late apoptosis. Cell cycle analysis on HepG2 cells showed that HepTH1-5 was able to block cell at G2/M phase significantly but not in HeLa while methotrexate arrest cells at G0/G1 phase. This data revealed that apoptosis effect of HepTH1-5 and methotrexate in cell cycle might occur at different mechanism. Taking all the data together, it was found that HepTH1-5 significantly triggers apoptosis in cancerous cells and it shows that this peptide could potentially be developed as anticancer agent.
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| title |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| title_full |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| title_fullStr |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| title_full_unstemmed |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| title_short |
Induction of Apoptosis and G2/M Phase Cell Cycle Arrest by Antimicrobial Peptide HepTH1-5
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| title_sort |
induction of apoptosis and g2/m phase cell cycle arrest by antimicrobial peptide hepth1-5
|