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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
Main Authors: Hsu, Jung-Chieh, Lin, Li-Ching, Tzen, Jason T.C., Chen, Jyh-Yih
Format: Article
Language:English
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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.
ISSN:0196-9781
1873-5169
DOI:10.1016/j.peptides.2011.02.013