Xiao-Jun Tang1, Qing-Hua Zhou, Shang-Fu Zhang, Lun-Xu Liu. 1. Sichuan Provincial Key Laboratory of Lung Cancer Molecular Biology, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, P.R.China.
Abstract
BACKGROUND & OBJECTIVE: Recently, studies showed nm23, E-cadherin, and Catenins play important roles in cellular signal transduction, which enhance complexity of their functions in tumor metastasis and can partly explain the diversity of the results from different studies. This study was to investigate correlations of expressions of nm23, E-cadherin, and beta-Catenin in non-small cell lung cancer (NSCLC) to metastasis and prognosis, and their interrelations. METHODS: Expressions of nm23, E-cadherin, and beta-Catenin in 112 specimens of NSCLC and 30 specimens of benign pulmonary lesion were detected by SP immunohistochemistry. RESULTS: The expressions of nm23, E-cadherin and beta-Catenin were significantly weaker in NSCLC tissues than in adjacent non-cancerous tissues, and benign pulmonary tissues (53.0% vs. 64.8%, and 76.9%, P < 0.01; 53.1% vs. 79.7%, and 83.5%, P < 0.01; and 47.2% vs. 80.6%, and 85.6%, P < 0.01), significantly weaker in NSCLC tissues with lymph node metastasis than in those without metastasis (48.0% vs. 65.0%, P < 0.01; 47.3% vs. 60.5%, P < 0.01; and 41.8% vs. 60.3%, P < 0.01), and significantly weaker in NSCLC tissues of stage III-IV than in those of stage I-II (44.8% vs. 67.2%, P < 0.01; 46.6% vs. 64.3%, P < 0.01; 38.1% vs. 63.1%, P < 0.01). The 5-year survival rates of patients with weak expressions of nm23, E-cadherin, and beta-Catenin were significantly lower than those of patients with strong expressions (3.6% vs. 39.3%, P < 0.01; 6.8% vs. 35.8%, P < 0.01; and 3.8% vs. 37.3%, P < 0.01). CONCLUSIONS: Down-regulations of nm23, E-cadherin, and beta-catenin closely relate to metastasis of NSCLC. Detection of nm23, E-cadherin, and beta-Catenin might be helpful to predict prognosis of NSCLC patients.
BACKGROUND & OBJECTIVE: Recently, studies showed nm23, E-cadherin, and Catenins play important roles in cellular signal transduction, which enhance complexity of their functions in tumor metastasis and can partly explain the diversity of the results from different studies. This study was to investigate correlations of expressions of nm23, E-cadherin, and beta-Catenin in non-small cell lung cancer (NSCLC) to metastasis and prognosis, and their interrelations. METHODS: Expressions of nm23, E-cadherin, and beta-Catenin in 112 specimens of NSCLC and 30 specimens of benign pulmonary lesion were detected by SP immunohistochemistry. RESULTS: The expressions of nm23, E-cadherin and beta-Catenin were significantly weaker in NSCLC tissues than in adjacent non-cancerous tissues, and benign pulmonary tissues (53.0% vs. 64.8%, and 76.9%, P < 0.01; 53.1% vs. 79.7%, and 83.5%, P < 0.01; and 47.2% vs. 80.6%, and 85.6%, P < 0.01), significantly weaker in NSCLC tissues with lymph node metastasis than in those without metastasis (48.0% vs. 65.0%, P < 0.01; 47.3% vs. 60.5%, P < 0.01; and 41.8% vs. 60.3%, P < 0.01), and significantly weaker in NSCLC tissues of stage III-IV than in those of stage I-II (44.8% vs. 67.2%, P < 0.01; 46.6% vs. 64.3%, P < 0.01; 38.1% vs. 63.1%, P < 0.01). The 5-year survival rates of patients with weak expressions of nm23, E-cadherin, and beta-Catenin were significantly lower than those of patients with strong expressions (3.6% vs. 39.3%, P < 0.01; 6.8% vs. 35.8%, P < 0.01; and 3.8% vs. 37.3%, P < 0.01). CONCLUSIONS: Down-regulations of nm23, E-cadherin, and beta-catenin closely relate to metastasis of NSCLC. Detection of nm23, E-cadherin, and beta-Catenin might be helpful to predict prognosis of NSCLCpatients.