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Characteristics of the antitumor activities in tumor cells and modulation of the inflammatory response in RAW264.7 cells of a novel antimicrobial peptide, chrysophsin-1, from the red sea bream ( Chrysophrys major)
► Chrysophsin-1 induced cell membrane rupture much like a lytic peptide. ► Chrysophsin-1 induced necrosis with high-concentration treatment. ► Chrysophsin-1 inhibited tumor cell growth. ► The modulatory activity of the inflammatory response and antitumor activity of chrysophsin-1 were examined. The...
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Published in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2011-05, Vol.32 (5), p.900-910 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | ► Chrysophsin-1 induced cell membrane rupture much like a lytic peptide. ► Chrysophsin-1 induced necrosis with high-concentration treatment. ► Chrysophsin-1 inhibited tumor cell growth. ► The modulatory activity of the inflammatory response and antitumor activity of chrysophsin-1 were examined.
The antimicrobial peptide, chrysophsin-1, exhibits antimicrobial activities with similar efficiencies for both gram-negative and gram-positive bacteria. In this study, we examined the antitumor activity and modulation of the inflammatory response of a synthetic chrysophsin-1 peptide. In vitro results showed that chrysophsin-1 had greater inhibitory effects against human fibrosarcoma (HT-1080), histiocytic lymphoma (U937), and epithelial carcinoma (HeLa) cells. LDH release by HeLa cells was comparable to that of an MTS assay after treatment with 1.5–3
μg/ml chrysophsin-1 for 24
h. Under SEM and TEM observations, we found no intact cell membranes after chrysophsin-1 treatment of HeLa cells for 8
h. The suggested mechanism of the cytotoxic activity of chrysophsin-1 was disruption of cancer cell membranes. In addition, we also examined caspase-3, -8, and -9 activities by Western blotting; the results excluded the participation of apoptosis in chrysophsin-1's effect on HeLa cells. Stimulation by lipopolysaccharide induced tumor necrosis factor (TNF)-α which was able to modulate chrysophsin-1 treatment of RAW264.7 cells and inhibited endogenous TNF-α release but did not block its secretion. With data from this study, we demonstrate that chrysophsin-1 has antimicrobial and antitumor activities and modulates the inflammatory response in RAW264.7 cells. |
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ISSN: | 0196-9781 1873-5169 |
DOI: | 10.1016/j.peptides.2011.02.013 |