WIF-1 gene inhibition and Wnt signal transduction pathway activation in NSCLC tumorigenesis

The aim of the present study is to explore the differential expression of key molecules associated with Wnt signaling in both clinical non-small cell lung cancer (NSCLC) tissue and adjacent normal lung tissue, and to discuss the tumorigenic role of the activation of Wnt signaling pathways in NSCLC. A total of 52 NSCLC patients were employed in the present study. Lung cancer tissue samples and paracarcinoma tissue samples were obtained from these patients, who had undergone surgical resection of their primary cancer. The cases were diagnosed by hematoxylin and eosin staining. Using reverse transcription-quantitative polymerase chain reaction and immunohistochemical straining, the messenger RNA ( mRNA) and protein expression levels of Wnt inhibitory factor-1 (WIF-1) and important molecules associated with Wnt signaling pathways were detected. Compared with normal tissues, a marked decreased in the mRNA and protein expression levels of WIF-1, and an increase in beta-catenin and cyclin D1 expression, were observed in tumor tissues. This suggests that the activation of the Wnt/beta-catenin signaling pathway may be closely associated with lymph nodal metastasis and lower pathological classification. However, no obvious difference could be observed in adenomatous polyposis coli (APC) expression levels between lung cancer tissues and adjacent tissues to the carcinoma. The activation of the Wnt/beta-catenin signaling pathway in NSCLC could be initiated by WIF-1gene inhibition without APC expression changes, and this may be different to the mechanism in other tumors.