Abstract
Studies on the anticancer mechanism of peptide P18 in human leukemia K562 cells revealed that P18 causes the death of most K562 cells by depolarizing plasma membrane potential and enhancing membrane permeability, rather than activating the classical apoptosis pathway. The mechanistic studies indicate that disrupting plasma membrane is an effective approach to kill cancer cells and help design more effective peptide analogues in future cancer therapies.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Antibiotics, Antineoplastic / chemical synthesis
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Antibiotics, Antineoplastic / chemistry
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Antibiotics, Antineoplastic / pharmacology*
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Antimicrobial Cationic Peptides / chemical synthesis
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Antimicrobial Cationic Peptides / chemistry
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Antimicrobial Cationic Peptides / pharmacology*
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Cell Death / drug effects
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Cell Membrane Permeability / drug effects
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Cell Survival / drug effects
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Humans
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K562 Cells
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Leukemia / drug therapy*
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Membrane Potentials / drug effects
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Mice
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Molecular Sequence Data
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NIH 3T3 Cells
Substances
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Antibiotics, Antineoplastic
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Antimicrobial Cationic Peptides
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P18 antimicrobial peptide