三裂叶蜣螂CopA3 肽通过 caspase 非依赖性途径诱导人白血病细胞凋亡。
CopA3 peptide from Copris tripartitus induces apoptosis in human leukemia cells via a caspase-independent pathway.
机构信息
Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Daejin University, Pocheon 487-711, South Korea.
出版信息
BMB Rep. 2012 Feb;45(2):85-90. doi: 10.5483/BMBRep.2012.45.2.85.
PMID:22360885
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.
摘要
我们之前的研究表明，CopA3 是一种二硫键二聚体的 coprisin 肽类似物（LLCIALRKK），具有抗菌活性。在这项研究中，我们评估了 CopA3 是否会在各种哺乳动物细胞系中引起细胞毒性。CopA3 选择性地导致 Jurkat T、U937 和 AML-2 细胞（人白血病细胞）的细胞活力明显下降，但对 Caki 或 Hela 细胞没有细胞毒性。凋亡的标志物——DNA 片段化也在白血病细胞系中得到证实，但在其他细胞中没有。CopA3 诱导白血病细胞凋亡是通过凋亡诱导因子 (AIF) 介导的，表明诱导了一种 caspase 非依赖性信号通路。
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