Xu Hong-Tao, Li Qing-Chang, Zhang Yong-Xing, Zhao Yue, Liu Yang, Yang Zhi-Qiang, Wang En-Hua
Department of Pathology, College of Basic Medical Sciences, China Medical University, Shenyang 110001, China.
Folia Histochem Cytobiol. 2008;46(3):315-21. doi: 10.2478/v10042-008-0057-9.
The interaction of connexin 43 and E-cadherin may play an important role in carcinogenesis and malignant behaviour of tumours. In this study, we examined the relationship between connexin 43 and E-cadherin in human non-small cell lung cancers (NSCLC). Expression levels of connexin 43 and E-cadherin were examined in 107 NSCLC specimens by immunohistochemistry. The connexin 43 gene was transfected into lung cancer LH7 cells. The protein localizations and levels of connexin 43 and E-cadherin were detected using immunofluorescence staining and western blot. Cell cycle and proliferation of lung cancer cells were examined using flow cytometry and MTT. We found that reduced expression of both connexin 43 and E-cadherin significantly correlated to poor differentiation, advanced TNM stage, and lymph note metastasis of NSCLCs. Connexin 43 and E-cadherin expression significantly correlated with each other. Over-expression of connexin 43 significantly induced E-cadherin expression. Moreover, connexin 43-transfected LH7 cells showed significantly decreased cell proliferation. The percentage of cells in G1 phase increased, while the number of cells in S and G2 phases significantly decreased. We concluded that concurrent reduction of connexin 43 and E-cadherin may contribute to the development of lung cancer. Connexin 43 may induce E-cadherin expression and inhibit cell proliferation and progression of lung cancer.
连接蛋白43与E-钙黏蛋白的相互作用可能在肿瘤的发生及恶性行为中发挥重要作用。在本研究中,我们检测了人非小细胞肺癌(NSCLC)中连接蛋白43与E-钙黏蛋白之间的关系。采用免疫组织化学法检测了107例NSCLC标本中连接蛋白43和E-钙黏蛋白的表达水平。将连接蛋白43基因转染至肺癌LH7细胞。采用免疫荧光染色和蛋白质印迹法检测连接蛋白43和E-钙黏蛋白的蛋白质定位及水平。采用流式细胞术和MTT法检测肺癌细胞的细胞周期和增殖情况。我们发现,连接蛋白43和E-钙黏蛋白的表达降低均与NSCLC的低分化、TNM分期进展及淋巴结转移显著相关。连接蛋白43和E-钙黏蛋白的表达显著相关。连接蛋白43的过表达显著诱导E-钙黏蛋白的表达。此外,转染连接蛋白43的LH7细胞显示细胞增殖显著降低。G1期细胞百分比增加,而S期和G2期细胞数量显著减少。我们得出结论,连接蛋白43和E-钙黏蛋白的同时降低可能促进肺癌的发展。连接蛋白43可能诱导E-钙黏蛋白表达并抑制肺癌细胞的增殖及进展。