Loss of CD10/NEP Expression in the Pulmonary Carcinogenesis / Journal of the Korean Cancer Association, 대한암학회지

ABSTRACT

PURPOSES: The cell surface metalloproteinase CD10/ neutral endopeptidase 24.11 (NEP) hydrolyzes a variety of peptide substrates and reduces cellular responses to specific peptide hormones. CD10/NEP has been recognized as modulating peptide-mediated proliferation of lung carcinomas and the normal airway epithelium. The purposes of this study are to evaluate the expression of CD10/NEP in human lung cancers, including non- small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC), and to correlate its expression with several clinicopathologic parameters, including proliferative activity. MATERIALS AND METHODS: CD10/NEP expression and proliferative activity were evaluated by immunohisto chemistry in 55 formalin-fixed and paraffin-embedded NSCLC and SCLC specimens, using anti-Human CD10/ NEP and Ki-67 primary antibodies. The correlations between CD10/NEP expression and either Ki-67 proliferative activity or several clinicopathologic parameters were analyzed by chi-square test or Fisher's exact test. RESULTS: Most NSCLC (76%) and SCLC (80%) cases showed loss of CD10/NEP expression in the tumor cells, whereas the bronchial and alveolar epithelia and stromal fibroblasts in the adjacent healthy lung revealed strong expression of CD10/NEP. Its expression was not correlated with proliferative activity or any of the clinicopathologic parameters except for age. Only in terms of topographical expression was CD10/NEP expression found to be inversely correlated with Ki-67 proliferative activity. CONCLUSION: These results suggest that loss of CD10/ NEP expression may be important in the pulmonary carcinogenesis of both NSCLCs and SCLCs, which is topographically related to NSCLC proliferative activity, especially in the squamous cell type.