错配修复蛋白与上皮间质转化标志物在大肠癌中表达及意义
| 作者: |
1吴建龙,
1刘建伟,
1刘海丽,
1郁葱颖,
1申志华,
1段庆华,
1尹位红,
1王海凤
1 承德市中心医院病理科，河北 承德 067000 |
| 通讯: |
刘海丽
Email: liuhaili2011@163.com |
| DOI: | 10.3978/j.issn.2095-6959.2018.08.008 |
| 基金: | 承德市科技计划项目(201701A018)。 |
摘要
目的：探讨错配修复(mismatch repair，MMR)蛋白与上皮间质转化(epithelial mesenchymal transition，EMT)标志物在大肠癌中的表达及意义，并分析二者关系。方法：采用免疫组织化学方法标记大肠癌组织中MMR蛋白(MSH1，MSH2，MSH6及PMS2)及EMT标志物(E-cadherin和Vimentin)的表达。MSH1，MSH2，MSH6及PMS2四种蛋白中的1种及以上表达缺失判定为错配修复基因缺陷(deficient mismatch repair，dMMR)，全部表达判定为错配基因完整(proficient mismatch repair，pMMR)。结果：242例大肠癌中186例pMMR，MMR蛋白表达率为76.86%；56例dMMR，MMR蛋白缺失率为23.14%。且大肠癌中dMMR与发病部位差异有统计学意义，68例右半结肠癌中31例dMMR(45.59%)，118例左半结肠癌中18例dMMR(15.25%)，56例直肠癌中7例dMMR(12.50%)。并且有淋巴结转移组和侵透肌层组dMMR要明显低于无淋巴结转移组及侵犯肌层组(P<0.05)。242例大肠癌中E-cadherin表达189例(78.10%)，低于癌旁组织(98.76%)，差异有统计学意义(P<0.05)；Vimentin表达38例(15.70%)，明显高于癌旁组织(0%)，差异有统计学意义(P<0.05)。低分化大肠癌、有淋巴结转移组及侵透肌层组E-cadherin的表达明显低于高-中分化大肠癌、无淋巴结组及侵犯肌层组(P<0.05)。而Vimentin的表达则相反(P<0.05)。发病部位上右半结肠癌E-cadherin的表达要高于左半结肠及直肠癌，Vimentin右半结肠癌的表达低于左半结肠癌及直肠癌(P<0.05)。结论：错配修复蛋白状态和EMT过程与大肠癌的发生及进展有关，影响其预后，提示存在MMR蛋白缺失状态的大肠癌其EMT过程也不明显。
关键词：
大肠癌；错配修复蛋白；上皮间质转化
Expression and significance of mismatch repair protein and epithelial mesenchymal transition marker in colorectal cancer
CorrespondingAuthor: LIU Haili Email: liuhaili2011@163.com
DOI: 10.3978/j.issn.2095-6959.2018.08.008
Foundation: This work was supported by Chengde Science and Technology Plan Project, China (201701A018).
Abstract
Objective: To investigate the expression and significance of mismatch repair protein (MMR) and epithelial mesenchymal transition (EMT) markers in colorectal cancer, and to analyze their relationships. Methods: The expressions of mismatch repair proteins (MSH1, MSH2, MSH6, and PMS2) and E-cadherin and Vimentin in colorectal cancer tissues were marked by immunohistochemistry. The deletion of one or more of MSH1, MSH2, MSH6, and PMS2 proteins was determined as deficient mismatch repair (dMMR), and all expressions were judged as proficient mismatch repair (pMMR). Results: In 242 cases of colorectal cancer, there were 186 cases of pMMR, the expression rate of MMR protein was 76.86%, and in 56 cases of dMMR, the rate of deletion of MMR protein was 23.14%. And there were differences in dMMR and pathogenesis in colorectal cancer. There were 31 cases of dMMR (45.59%) in 68 cases of right colon cancer, 18 cases of dMMR (15.25%) in 118 cases of left colon cancer, and 7 cases of dMMR (12.50%) in 56 cases of rectal cancer. The dMMR in the lymph node metastasis group and the penetrating muscle group was significantly lower than that in the group without lymph node metastasis and in the muscle invading group. 189 cases (78.10%) of colorectal carcinoma had E-cadherin expression, which was lower than that in paraneoplastic tissue (98.76%), the difference was statistically significant (P<0.05); Vimentin expression in 38 cases (15.70%) was significantly higher than paraneoplastic tissue (0%), the difference was statistically significant (P<0.05). The expression of E-cadherin in poorly differentiated colorectal cancer, lymph node metastasis group, and penetrate muscle layer was significantly lower than that in high-grade differentiated colorectal cancer, no lymph node group, and muscle infiltration group (P<0.05). The expression was opposite (P<0.05). The expression of E-cadherin in the right colon was higher than that in the left colon and rectal cancer. The expression of Vimentin in colon cancer was lower than that in the left colon and rectal carcinoma (P<0.05). Conclusion: The status of mismatch repair protein and the process of epithelial-mesenchymal transition are related to the occurrence and progression of colorectal cancer, and affect its prognosis. It also suggests that the presence of MMR protein-deficient colorectal cancer has no obvious epithelial-mesenchymal transition.
Keywords：
colorectal cancer; mismatch repair protein; epithelial-mesenchymal transition