Anticancer mechanism of peptide P18 in human leukemia K562 cells

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 indicat...

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Veröffentlicht in:	Organic & biomolecular chemistry 2010-01, Vol.8 (5), p.984-987
Hauptverfasser:	Tang, Chengkang, Shao, Ximing, Sun, Binbin, Huang, Wenli, Qiu, Feng, Chen, Yongzhu, Shi, Ying-kang, Zhang, Er-yong, Wang, Chen, Zhao, Xiaojun
Format:	Artikel
Sprache:	eng
Schlagworte:	Amino Acid Sequence Animals Antibiotics, Antineoplastic - chemical synthesis Antibiotics, Antineoplastic - chemistry Antibiotics, Antineoplastic - pharmacology Antimicrobial Cationic Peptides - chemical synthesis Antimicrobial Cationic Peptides - chemistry Antimicrobial Cationic Peptides - pharmacology Cell Death - drug effects Cell Membrane Permeability - drug effects Cell Survival - drug effects Humans K562 Cells Leukemia - drug therapy Membrane Potentials - drug effects Mice Molecular Sequence Data NIH 3T3 Cells
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Zusammenfassung:	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.
ISSN:	1477-0520 1477-0539
DOI:	10.1039/b920762g