Department of Pathology, Juntendo University School of Medicine, Tokyo, Japan.
Cancer Sci. 2010 Apr;101(4):969-74. doi: 10.1111/j.1349-7006.2009.01463.x. Epub 2009 Dec 9.
Mesothelioma is an aggressive cancer often caused by chronic asbestos exposure, and its prognosis is very poor despite the therapies currently used. Due to the long latency period between asbestos exposure and tumor development, the worldwide incidence will increase substantially in the next decades. Thus, novel effective therapies are warranted to improve the prognosis. The ERC/mesothelin gene (MSLN) is expressed in wide variety of human cancers, including mesotheliomas, and encodes a precursor protein cleaved by proteases to generate C-ERC/mesothelin and N-ERC/mesothelin. In this study, we investigated the antitumor activity of C-ERC/mesothelin-specific mouse monoclonal antibody, 22A31, against tumors derived from a human mesothelioma cell line, ACC-MESO-4, in a xenograft experimental model using female BALB/c athymic nude mice. Treatment with 22A31 did not inhibit cell proliferation of ACC-MESO-4 in vitro; however, therapeutic treatment with 22A31 drastically inhibited tumor growth in vivo. 22A31 induced antibody-dependent cell-mediated cytotoxicity by natural killer (NK) cells, but not macrophages, in vitro. Consistently, the F(ab')(2) fragment of 22A31 did not inhibit tumor growth in vivo, nor did it induce antibody-dependent cell mediated cytotoxicity (ADCC) in vitro. Moreover, NK cell depletion diminished the antitumor effect of 22A31. Thus, 22A31 induced NK cell-mediated ADCC and exerted antitumor activity in vivo. 22A31 could have potential as a therapeutic tool to treat C-ERC/mesothelin-expressing cancers including mesothelioma.
间皮瘤是一种侵袭性癌症,通常由慢性石棉暴露引起,尽管目前使用了多种治疗方法,但预后仍很差。由于石棉暴露与肿瘤发展之间存在很长的潜伏期,因此在未来几十年,全球发病率将大幅增加。因此,需要新的有效治疗方法来改善预后。ERC/间皮素基因(MSLN)在广泛的人类癌症中表达,包括间皮瘤,并编码一种前体蛋白,该蛋白被蛋白酶切割生成 C-ERC/间皮素和 N-ERC/间皮素。在这项研究中,我们使用雌性 BALB/c 无胸腺裸鼠的异种移植实验模型,研究了 C-ERC/间皮素特异性小鼠单克隆抗体 22A31 对源自人间皮瘤细胞系 ACC-MESO-4 的肿瘤的抗肿瘤活性。22A31 治疗并未抑制 ACC-MESO-4 在体外的细胞增殖;然而,22A31 的治疗性治疗在体内显著抑制了肿瘤生长。22A31 在体外诱导自然杀伤(NK)细胞而非巨噬细胞的抗体依赖性细胞介导的细胞毒性(ADCC)。一致地,22A31 的 F(ab')(2)片段在体内不抑制肿瘤生长,也不在体外诱导 ADCC。此外,NK 细胞耗竭减弱了 22A31 的抗肿瘤作用。因此,22A31 诱导 NK 细胞介导的 ADCC,并在体内发挥抗肿瘤活性。22A31 可能成为治疗包括间皮瘤在内的 C-ERC/间皮素表达癌症的治疗工具。