Prognostic value and immune infiltration of the NEK family in clear cell renal cell carcinoma

Background Clear cell renal cell carcinoma (ccRCC) is a fatal urological malignancy, and surgery remains the primary treatment. Members of the never in mitosis gene A (NIMA)-related kinase (NEK) family have been found to participate in the progression of several cancers and could be used as target genes to treat corresponding diseases. Nonetheless, the prognostic value and immune infiltration levels of NEK family genes in ccRCC remain unknown. Methods Gene Set Cancer Analysis (GSCA), Tumor Immune Estimation Resource (TIMER), and Gene Expression Profiling Interactive Analysis (GEPIA) databases were utilized to examine the differential expression of NEK family genes in ccRCC, and the Kaplan-Meier plotter was utilized to analyze the prognosis. The Search Tool for Retrieval of Interacting Genes(STRING) database was used to construct a protein-protein interaction network. Analysis of function was performed by the Sangerbox tool. Finally, the relationship between NEK family genes and immune cell infiltration was explored using the TIMER database. Results Transcriptional levels of NEK2, NEK3, NEK5, NEK6, and NEK11 significantly differed between ccRCC and normal tissues. Moreover, there was a significant correlation between NEK1, NEK2, NEK4, NEK8, NEK9, and NEK10 and their clinicopathological stages in patients with ccRCC. Based on survival analysis, ccRCC patients with high transcriptional levels of NEK2, NEK3, NEK8, and NEK10 and low transcriptional levels of NEK1, NEK4, NEK5, NEK6, NEK7, NEK9, NEK11 had shorter survival times. Additionally, a significant relationship was observed between immune cell infiltration and NEK family members. Conclusions These results indicate that NEK family members are significantly differentially expressed in ccRCC, and a significant correlation exists between the NEK family and prognosis and immune infiltration. NEK family members may act as therapeutic targets and prognostic indicators in ccRCC.