Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression
Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression
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DOI：
10.1016/j.canlet.2008.08.012
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发表时间：
2009-01-18
期刊：
影响因子：
9.7
通讯作者：
Topham, Matthew K.
中科院分区：
文献类型：
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作者：
Al-Salihi, Mazin A.;Pearman, A. Terrece;Topham, Matthew K.
我们产生了在结肠上皮中表达考克斯-2转基因的小鼠，发现它们没有发生自发性结肠肿瘤。但是当用氧化偶氮甲烷（一种结肠致癌物）治疗时，考克斯-2小鼠的肿瘤负荷比野生型小鼠高。肿瘤前病变的数量没有变化，表明考克斯-2不影响肿瘤的发生。与野生型小鼠相比，考克斯-2转基因小鼠的肿瘤具有更高水平的磷酸化表皮生长因子受体和Akt。总的来说，我们的数据表明，考克斯-2促进结肠肿瘤的进展，但不启动，它这样做，部分通过激活EGFR和Akt信号通路。(C)2008爱思唯尔爱尔兰有限公司保留所有权利。
We generated mice expressing a COX-2 transgene in colon epithelium and found that they did not develop spontaneous colon tumors. But when treated with azoxymethane, a colon carcinogen, COX-2 mice had a higher tumor load compared to wild-type mice. There was no change in the number of pre-neoplastic lesions, indicating that COX-2 does not affect tumor initiation. Tumors in the COX-2 transgenic mice had higher levels of phosphorylated epidermal growth factor receptor and Akt compared to wild-type mice. Collectively, our data indicate that COX-2 promotes colon tumor progression, but not initiation, and it does so, in part, by activating EGFR and Akt signaling pathways. (C) 2008 Elsevier Ireland Ltd. All rights reserved.