The role of the Wnt signalling pathway in colorectal tumorigenesis
The role of the Wnt signalling pathway in colorectal tumorigenesis
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DOI：
10.1042/bst0330672
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发表时间：
2005-08-01
影响因子：
3.9
通讯作者：
Behrens, J
中科院分区：
文献类型：
--
作者：
Behrens, J
结直肠癌(CRC)是西方国家癌症相关死亡的第二大原因。结直肠癌起源于结直肠上皮，是明确的癌基因和肿瘤抑制基因的遗传改变累积的结果。肿瘤抑制基因APC(腺瘤性息肉病)基因的突变发生在结直肠癌的早期，导致Wnt通路成分β-catenin的稳定和Wnt信号的结构性激活。稳定β-连环蛋白的突变也可以导致其积累，使其有资格成为原癌基因。在这里，我将总结在WRIT信号中发生的生化相互作用，并描述Wnt途径组件的改变如何导致CRC。
Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes. Mutations in the tumour suppressor APC (adenomatous polyposis coli) genes occur early in the development of CRC and lead to the stabilization of the Wnt pathway component beta-catenin and to the constitutive activation of Wnt signalling. Stabilizing mutations of beta-catenin can also lead to its accumulation, qualifying beta-catenin as a proto-oncogene. Here I will summarize the biochemical interactions occurring in Writ signalling and describe how alterations in Wnt pathway components lead to CRC.