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 indicate that disrupting plasma membrane is an effective approach to kill cancer cells and help design more effective peptide analogues in future cancer therapies.
Tang
Chengkang
C
Institute for Nanobiomedical Technology and Membrane Biology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Shao
Ximing
X
Sun
Binbin
B
Huang
Wenli
W
Qiu
Feng
F
Chen
Yongzhu
Y
Shi
Ying-kang
YK
Zhang
Er-yong
EY
Wang
Chen
C
Zhao
Xiaojun
X
D000595:Amino Acid Sequence; D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology*; D023181:Antimicrobial Cationic Peptides / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D020014:K562 Cells; D007938:Leukemia / Q000188:drug therapy*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008969:Molecular Sequence Data; D041681:NIH 3T3 Cells
D000903:Antibiotics, Antineoplastic; D023181:Antimicrobial Cationic Peptides; C447608:P18 antimicrobial peptide