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Loss of CD10/NEP Expression in the Pulmonary Carcinogenesis
Purpose:
S: 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.
Insights
Loss of CD10/neutral endopeptidase 24.11 (NEP) expression in lung cancer cells may drive pulmonary carcinogenesis. This loss is topographically linked to non-small cell lung carcinoma (NSCLC) proliferation, particularly in squamous cell types.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- CD10/neutral endopeptidase 24.11 (NEP) is a cell surface metalloproteinase modulating peptide hormone responses.
- CD10/NEP influences peptide-mediated proliferation in lung carcinomas and airway epithelium.
Purpose of the Study:
- To evaluate CD10/NEP expression in non-small cell lung carcinoma (NSCLC) and small cell lung carcinoma (SCLC).
- To correlate CD10/NEP expression with clinicopathologic parameters and proliferative activity.
Main Methods:
- Immunohistochemistry used to assess CD10/NEP and Ki-67 expression in 55 NSCLC and SCLC specimens.
- Chi-square or Fisher's exact tests analyzed correlations between CD10/NEP, Ki-67, and clinicopathologic parameters.
Main Results:
- Most NSCLC (76%) and SCLC (80%) cases exhibited loss of CD10/NEP expression in tumor cells.
- CD10/NEP expression was strong in normal bronchial/alveolar epithelia and stromal fibroblasts.
- CD10/NEP expression showed no correlation with proliferative activity or most clinicopathologic parameters, except age.
Conclusions:
- Loss of CD10/NEP expression may play a role in pulmonary carcinogenesis for both NSCLC and SCLC.
- Topographical CD10/NEP expression is inversely correlated with NSCLC proliferative activity, especially in squamous cell carcinoma.
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