Brief Article
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World J Gastroenterol. Jan 7, 2014; 20(1): 250-257
Published online Jan 7, 2014. doi: 10.3748/wjg.v20.i1.250
Epithelial-mesenchymal transition in colorectal cancer tissue of patients with Lynch syndrome
Guo-Li Gu, Xiao-Quan Zhu, Xue-Ming Wei, Li Ren, De-Chang Li, Shi-Lin Wang
Guo-Li Gu, Xue-Ming Wei, Shi-Lin Wang, Department of General Surgery, the Air Force General Hospital PLA, Beijing 100142, China
Xiao-Quan Zhu, the Affiliated Hospital of Aviation Medical Institute, PLA Air Force, Beijing 100142, China
Li Ren, De-Chang Li, Department of Pathology, the Air Force General Hospital PLA, Beijing 100142, China
Author contributions: Gu GL and Wei XM designed the research; Gu GL, Ren L and Li DC performed the research; Gu GL, Zhu XQ and Ren L collected and analyzed the data; Gu GL wrote the paper; and Wei XM and Wang SL revised the paper.
Supported by Capital Citizen Health Cultivation Project, No. Z131100004013021; and General Projects of the Chinese PLA “Twelfth Five-Year” Logistics Research Subject, No. CWS11J193
Correspondence to: Xue-Ming Wei, Professor, Department of General Surgery, the Air Force General Hospital PLA, No.30, Fucheng Road, Haidian District, Beijing 100142, China. kzggl@163.com
Telephone: +86-10-66928302 Fax: +86-10-66928302
Received: September 9, 2013
Revised: October 29, 2013
Accepted: November 18, 2013
Published online: January 7, 2014
Core Tip

Core tip: As a subgroup of colorectal carcinoma (CRC), Lynch syndrome presents better prognosis than sporadic CRC for less invasion and metastasis. Our study found epithelial-mesenchymal transition may play an important role in the development and progression of Lynch syndrome. Lynch syndrome was caused by the mutations of mismatch repair genes, which also beget the mutational inactivation of transforming growth factor-β type II receptor. Therefore, the colorectal cancer of Lynch syndrome can escape the inhibitory effect of transforming growth factor-β type 1 (TGFβ1). However TGFβ1 can up-regulate the expression of matrix metalloproteinase-7 and down-regulate the expression of tissue inhibitor of metalloproteinase-2 in tumors by disassembling the E-cadherin/β-catenin complex in the cytomembrane.