NEK2 Serves as a Novel Biomarker and Enhances the Tumorigenicity of Clear-CellRenal-Cell Carcinoma by Activating WNT/beta-Catenin Pathway

Objective. Currently, cumulative evidence has shown that loss of NEK2 function suppresses tumor growth. However, complete studies on the regulatory role of NEK2 in clear-cellrenal-cell carcinoma (ccRCC) are rarely reported. Methods. The GEPIA database was used for information mining to analyze the gene expression differences between ccRCC tumor and normal tissues. At the same time, we analyzed the protein expression of NEK2 in clinical ccRCC samples and ccRCC cell lines. We detected the effect of NEK2 on the biological behavior of ccRCC at the cell level and further verified the biological effect of NEK2 on ccRCC cells in vivo by nude mouse tumorigenesis experiment. The expression of WNT/beta-cateninpathway-related proteins and downstream proteins related to cell function were detected by Western blotting. Results. Using the GEPIA database, we observed that NEK2 expression level in ccRCC tissues was significantly higher than that in normal kidney tissues and was also related to tumor grade. The survival time of patients with ccRCC with high NEK2 expression was shorter than that of patients with low NEK2 expression. Compared with adjacent carcinoma and normal renal tubular epithelial cells, NEK2 levels were highly expressed in ccRCC tissues and ccRCC cell lines. NEK2 interference restrained ccRCC cell growth, migration, and invasion. NEK2 regulated the malignant behavior of ccRCC cells through the WNT/beta-catenin pathway. Nude mouse tumorigenesis assay results showed that the transplanted tumors from NEK2 silenced mice grew more slowly and were smaller in size than those from control mice. Conclusions. NEK2 elevation may be associated with poor prognosis in ccRCC, and NEK2 enhances ccRCC cell proliferation, migration, and invasion ability by activating the WNT/beta-catenin signaling pathway.