CopA3 peptide from Copris tripartitus induces apoptosis in human leukemia cells via a caspase-independent pathway.

Abstract

Our previous study demonstrated that CopA3, a disulfide dimer of the coprisin peptide analogue (LLCIALRKK), has antibacterial activity. In this study, we assessed whether CopA3 caused cellular toxicity in various mammalian cell lines. CopA3 selectively caused a marked decrease in cell viability in Jurkat T, U937, and AML-2 cells (human leukemia cells), but was not cytotoxic to Caki or Hela cells. Fragmentation of DNA, a marker of apoptosis, was also confirmed in the leukemia cell lines, but not in the other cells. CopA3-induced apoptosis in leukemia cells was mediated by apoptosis inducing factor (AIF), indicating induction of a caspase-independent signaling pathway.

• Authors: Bo Ram Kang, Ho Kim, Sung-Hee Nam, Eun-Young Yun, Seong-Ryul Kim, Mi-Young Ahn, Jong Soo Chang, Jae Sam Hwang
• Journal: BMB reports (BMB Rep) Vol. 45 Issue 2 Pg. 85-90 (Feb 2012) ISSN: 1976-670X [Electronic] Korea (South)
• PMID: 22360885 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Apoptosis Inducing Factor
• Insect Proteins
• coprisin peptide, Copris tripartitus
• Caspases

Topics

• Amino Acid Sequence
• Animals
• Apoptosis (drug effects)
• Apoptosis Inducing Factor (metabolism)
• Caspases (metabolism)
• Cell Line, Tumor
• Coleoptera (metabolism)
• HeLa Cells
• Humans
• Insect Proteins (chemical synthesis, therapeutic use, toxicity)
• Jurkat Cells
• Leukemia (drug therapy, metabolism)
• Signal Transduction