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基质金属蛋白酶激活的炭疽致死毒素在靶向肿瘤血管方面显示出高效力。

Matrix metalloproteinase-activated anthrax lethal toxin demonstrates high potency in targeting tumor vasculature.

作者信息

Liu Shihui, Wang Hailun, Currie Brooke M, Molinolo Alfredo, Leung Howard J, Moayeri Mahtab, Basile John R, Alfano Randall W, Gutkind J Silvio, Frankel Arthur E, Bugge Thomas H, Leppla Stephen H

机构信息

Laboratory of Bacterial Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892.

Oral and Pharyngeal Cancer Branch, NIDCR, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Biol Chem. 2008 Jan 4;283(1):529-540. doi: 10.1074/jbc.M707419200. Epub 2007 Nov 1.

Abstract

Anthrax lethal toxin (LT), a virulence factor secreted by Bacillus anthracis, is selectively toxic to human melanomas with the BRAF V600E activating mutation because of its proteolytic activities toward the mitogen-activated protein kinase kinases (MEKs). To develop LT variants with lower in vivo toxicity and high tumor specificity, and therefore greater potential for clinical use, we generated a mutated LT that requires activation by matrix metalloproteinases (MMPs). This engineered toxin was less toxic than wild-type LT to mice because of the limited expression of MMPs by normal cells. Moreover, the systemically administered toxin produced greater anti-tumor effects than wild-type LT toward human xenografted tumors. This was shown to result from its greater bioavailability, a consequence of the limited uptake and clearance of the modified toxin by normal cells. Furthermore, the MMP-activated LT had very potent anti-tumor activity not only to human melanomas containing the BRAF mutation but also to other tumor types, including lung and colon carcinomas regardless of their BRAF status. Tumor histology and in vivo angiogenesis assays showed that this anti-tumor activity is due largely to the indirect targeting of tumor vasculature and angiogenic processes. Thus, even tumors genetically deficient in anthrax toxin receptors were still susceptible to the toxin therapy in vivo. Moreover, the modified toxin also displayed lower immunogenicity compared with the wild-type toxin. All these properties suggest that this MMP-activated anti-tumor toxin has potential for use in cancer therapy.

摘要

炭疽致死毒素(LT)是炭疽芽孢杆菌分泌的一种毒力因子,由于其对丝裂原活化蛋白激酶激酶(MEK)具有蛋白水解活性,因此对具有BRAF V600E激活突变的人类黑色素瘤具有选择性毒性。为了开发体内毒性较低且肿瘤特异性高、因而具有更大临床应用潜力的LT变体,我们构建了一种需要基质金属蛋白酶(MMP)激活的突变型LT。由于正常细胞中MMP的表达有限,这种工程毒素对小鼠的毒性低于野生型LT。此外,全身给药的毒素对人异种移植肿瘤产生的抗肿瘤作用比野生型LT更强。这表明其具有更高的生物利用度,这是正常细胞对修饰毒素摄取和清除有限的结果。此外,MMP激活的LT不仅对含有BRAF突变的人类黑色素瘤具有非常强的抗肿瘤活性,而且对其他肿瘤类型,包括肺癌和结肠癌,无论其BRAF状态如何,都具有很强的抗肿瘤活性。肿瘤组织学和体内血管生成分析表明,这种抗肿瘤活性主要是由于对肿瘤血管和血管生成过程的间接靶向作用。因此,即使在体内基因上缺乏炭疽毒素受体的肿瘤仍然对毒素治疗敏感。此外,与野生型毒素相比,修饰后的毒素还表现出较低的免疫原性。所有这些特性表明这种MMP激活的抗肿瘤毒素具有用于癌症治疗的潜力。

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