Behrens J
Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nürnberg, Glueckstr. 6, D-91054 Erlangen, Germany.
Biochem Soc Trans. 2005 Aug;33(Pt 4):672-5. doi: 10.1042/BST0330672.
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 Wnt signalling and describe how alterations in Wnt pathway components lead to CRC.
在西方国家，结直肠癌（CRC）是癌症相关死亡的第二大原因。CRC起源于结直肠上皮，是特定原癌基因和肿瘤抑制基因中基因改变积累的结果。肿瘤抑制基因APC（腺瘤性息肉病 coli）的突变在CRC发展早期出现，并导致Wnt通路成分β-连环蛋白的稳定以及Wnt信号的组成性激活。β-连环蛋白的稳定突变也可导致其积累，使β-连环蛋白成为一种原癌基因。在此，我将总结Wnt信号中发生的生化相互作用，并描述Wnt通路成分的改变如何导致CRC。
