Department of Microbiology, College of Life Sciences, Cancer Hospital & Research Institute, Gwalior, MP, India; Department of Pharmaceutics, College of Pharmacy, PO Box 2457, King Saud University, Riyadh 11451, Saudi Arabia.
Cancer Lett. 2013 Dec 1;341(2):127-31. doi: 10.1016/j.canlet.2013.08.003. Epub 2013 Aug 7.
The recent demonstration of a role of Escherichia coli in the development of invasive carcinoma in mice ushers a new era of bacterial involvement in cancer etiology. It has been shown previously that the colonic mucosa of colorectal carcinoma (CRC) is exclusively colonized by intracellular E. coli instead of extracellular form found in normal colonic mucosa. Surprisingly, the DNA repair gene MUTYH, which is a homologue of the E. coli gene mutY, is responsible for CRC. The current paper discusses the potential role of mutY in CRC etiology and concludes that research in this area can bring together the diverse threads of the CRC etiology puzzle.
最近的研究表明，大肠杆菌在小鼠侵袭性癌中的作用，开启了细菌参与癌症病因学的新时代。此前已经表明，结直肠癌（CRC）的结肠黏膜仅被细胞内大肠杆菌定植，而不是正常结肠黏膜中发现的细胞外形式。令人惊讶的是，DNA 修复基因 MUTYH 是大肠杆菌基因 mutY 的同源物，它负责 CRC 的发生。本文讨论了 mutY 在 CRC 病因学中的潜在作用，并得出结论，该领域的研究可以将 CRC 病因学难题的各个方面联系起来。
