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首页> 外文期刊>Cancer science. >Susceptibility to natural killer cell‐mediated lysis of colon cancer cells is enhanced by treatment with epidermal growth factor receptor inhibitors through UL16‐binding protein‐1 induction
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Susceptibility to natural killer cell‐mediated lysis of colon cancer cells is enhanced by treatment with epidermal growth factor receptor inhibitors through UL16‐binding protein‐1 induction

机译：通过表皮生长因子受体抑制剂通过UL16结合蛋白-1诱导治疗，增强了自然杀伤细胞介导的结肠癌细胞裂解的敏感性

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AbstractWe have previously shown that inhibition of intracellular signaling pathways by treatment with quercetin induced the expression of natural killer cell group 2D (NKG2D) ligands on cancer cells and made the cells sensitive to natural killer (NK)-cell mediated cytotoxicity. In the present study, we investigated whether epidermal growth factor receptor (EGFR) inhibitors could induce the expression of NKG2D ligands in colon cancer cells. Treatment with EGFR inhibitors predominantly increased the levels of mRNA transcripts and surface protein of UL16-binding protein-1 (ULBP1) in various colon cancer cells, including KM12, Caco-2, HCT-15, and HT-29, which express EGFR, and increased susceptibility of these colon cancer cells to NK-92 cells. The expression of ULBP1 was not induced by inhibitors of nuclear factor-κB, phosphatidylinositol 3 kinase, and MAPK, but was induced by inhibitors of PKC, and the induction of ULBP1 expression with EGFR inhibitors was prevented by treatment with PMA in colon cancer cells. A transcription factor, activator protein-2 alpha (AP-2α), which has a suppressive effect on ULBP1 transcription, was prevented from binding to the ULBP1 promoter by treatment with EGFR inhibitors. The present study suggests that EGFR inhibitors can enhance the susceptibility to NK cell-mediated lysis of colon cancer cells by induction of ULBP1 via inhibition of the PKC pathway. (Cancer Sci 2012; 103: 7–16)
机译：摘要我们之前已经表明，通过槲皮素处理抑制细胞内信号传导途径可诱导癌细胞上自然杀伤细胞2D（NKG2D）配体的表达并使细胞对自然杀伤细胞（NK）介导的细胞毒性敏感。在本研究中，我们调查了表皮生长因子受体（EGFR）抑制剂是否可以诱导结肠癌细胞中NKG2D配体的表达。在各种表达EGFR的结肠癌细胞，包括KM12，Caco-2，HCT-15和HT-29的各种结肠癌细胞中，用EGFR抑制剂治疗主要提高了UL16结合蛋白1（ULBP1）的mRNA转录水平和表面蛋白水平，这些结肠癌细胞对NK-92细胞的敏感性增加。 ULBP1的表达不是由核因子-κB，磷脂酰肌醇3激酶和MAPK的抑制剂诱导的，而是由PKC的抑制剂诱导的，并且通过PMA处理在结肠癌细胞中阻止了EGFR抑制剂诱导的ULBP1表达。通过使用EGFR抑制剂可防止对ULBP1转录具有抑制作用的转录因子活化蛋白2α（AP-2α）与ULBP1启动子结合。本研究表明，EGFR抑制剂可通过抑制PKC途径来诱导ULBP1，从而增强结肠癌细胞对NK细胞介导的裂解的敏感性。 （《癌症科学》，2012年; 103：7-16）

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