C-terminal domain of human CAP18 antimicrobial peptide induces apoptosis in oral squamous cell carcinoma SAS-H1 cells
C-terminal domain of human CAP18 antimicrobial peptide induces apoptosis in oral squamous cell carcinoma SAS-H1 cells
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DOI：
10.1016/j.canlet.2004.04.006
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发表时间：
2004-08-30
期刊：
影响因子：
9.7
通讯作者：
Isogai, H
中科院分区：
文献类型：
--
作者：
Okumura, K;Itoh, A;Isogai, H
哺乳动物髓细胞和上皮细胞表达许多抗菌肽，有助于先天宿主防御入侵的微生物。在本研究中，研究了c端结构域的27-mer肽（hCAP18(109-135)）和抗菌肽human cathelicidin LL-37/human阳离子抗菌蛋白18（hCAP18）的类似物的杀肿瘤活性。体外实验结果显示，hCAP18（109-135）可诱导人口腔鳞癌（OSCC） SAS-H1细胞凋亡。hCAP18（109-135）在SAS-HI细胞中诱导线粒体去极化和凋亡，但在健康人牙龈成纤维细胞（HGF）和人角化细胞系HaCaT细胞中无诱导作用。caspase在hCAP18（109-135）诱导的SAS-H1细胞凋亡过程中未被激活。结果表明，hCAP18（109-135）在OSCC中可诱导caspase不依赖型细胞凋亡，而在正常细胞中则不能。因此，hCAP18（109-135）可作为治疗OSCC的有效抗肿瘤治疗剂。2004爱思唯尔爱尔兰有限公司版权所有。
Mammalian myeloid and epithelial cells express many antimicrobiotic peptides that contribute to innate host defense against invading microbes. In the present study, a 27-mer peptide of the C-terminal domain (hCAP18(109-135)) and analogs of the antimicrobial peptide human cathelicidin LL-37/human cationic antimicrobial protein 18 (hCAP18) were examined for tumoricidal activity. In vitro results showed that hCAP18(109-135) induced apoptosis in human oral squamous cell carcinoma (OSCC), SAS-H1 cells. The hCAP18(109-135) induced mitochondrial depolarization and apoptosis in SAS-HI cells, but not in healthy human gingival fibroblasts (HGF) and human keratinocyte line HaCaT cells. Caspases were not activated during hCAP18(109-135)-induced apoptosis in SAS-H1 cells. The results indicate that hCAP18(109-135) may induce caspase-independent apoptosis in OSCC but not in normal cells. hCAP18(109-135) can therefore be a useful anti-tumor therapeutic agent in the treatment of OSCC. (C) 2004 Elsevier Ireland Ltd. All rights reserved.