Abstract Herein, we aimed to investigate the functions of ADAMTS6 in colon cancer and its potential mechanism. Based on the data acquired from TCGA database, we revealed that ADAMTS6 was highly expressed in colon cancer tissues, and high expression of ADAMTS6 predicted worse prognosis in patients with colon cancer. Moreover, qRT-PCR demonstrated that the levels of ADAMTS6 were higher in colon cancer cell lines (NCI-H508, Caco-2, CW-2 and HCT 116) than that in normal control cell line CCD-18Co. Functional experiments displayed that depletion of ADAMTS6 repressed NCI-H508 cell growth, invasion and migration whilst overexpression of ADAMTS6 facilitated Caco-2 cell growth, invasion and migration. Moreover, ADAMTS6 silencing enhanced the protein expression of E-cadherin and reduced the levels of N-cadherin, Vimentin and Snail in NCI-H508 cells, whereas ADAMTS6 overexpression showed the counter effects in Caco-2 cells. The protein levels of p-AKT and p-p65 were decreased by depletion of ADAMTS6 in NCI-H508 cells, while their levels were enhanced by overexpression of ADAMTS6 in Caco-2 cells. These consequences indicated that the accelerating effect of ADAMTS6 on colon cancer cell growth, migration and invasion might be achieved by modulating EMT and AKT/NF-κB signaling pathway, offering important foundations for colon cancer treatment.

中文翻译：

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去整合素和金属蛋白酶的金属蛋白酶和血栓反应蛋白基序 6 作为结肠癌的新标志物：功能实验

摘要 本文旨在研究ADAMTS6在结肠癌中的功能及其潜在机制。基于从TCGA数据库获得的数据，我们发现ADAMTS6在结肠癌组织中高表达，ADAMTS6的高表达预示着结肠癌患者的预后较差。此外，qRT-PCR 表明结肠癌细胞系（NCI-H508、Caco-2、CW-2 和 HCT 116）中 ADAMTS6 的水平高于正常对照细胞系 CCD-18Co。功能实验表明，ADAMTS6 的消耗抑制了 NCI-H508 细胞的生长、侵袭和迁移，而 ADAMTS6 的过表达促进了 Caco-2 细胞的生长、侵袭和迁移。此外，ADAMTS6 沉默增强了 E-cadherin 的蛋白表达，降低了 NCI-H508 细胞中 N-cadherin、Vimentin 和 Snail 的水平，而 ADAMTS6 过表达在 Caco-2 细胞中显示出反作用。p-AKT 和 p-p65 的蛋白质水平因 NCI-H508 细胞中 ADAMTS6 的消耗而降低，而它们的水平因 Caco-2 细胞中 ADAMTS6 的过表达而增强。这些结果表明 ADAMTS6 对结肠癌细胞生长、迁移和侵袭的加速作用可能是通过调节 EMT 和 AKT/NF-κB 信号通路来实现的，为结肠癌的治疗提供了重要的基础。