OBJECTIVES: To investigate the role of Holliday cross-recognition protein (HJURP) in tumorigenesis, progression, and immunotherapy responses. METHODS: Bioinformatics approaches were used to analyze the expression level of HJURP in various cancers and its association with prognosis, clinical stage, and immune cell infiltration using TCGA, GTEx, SangerBox and TIMER 2.0 databases. LinkedOmics database was employed to investigate HJURP-related genes and their potential functions in kidney renal clear cell carcinoma (KIRC). The expression of HJURP in KIRC samples was examined with immunohistochemistry, Western blotting and qRT-PCR, and the effect of HJURP silencing on cell proliferation and migration was tested in cultured KIRC cells. RESULTS: HJURP was highly expressed in 26 cancers with negative correlations with the patients' survival outcomes in 5 cancers including KIRC (P<0.05). HJURP expression levels was strongly correlated with clinical stages and immune cell infiltration in the tumors. In KIRC, HJURP expression was significantly elevated (P<0.0001) and showed a positive correlation with TNM stage (P<0.05), overall stage (P<0.01) and immune cell infiltration. Gene Ontology (GO) functional analysis showed that HJURP is predominantly enriched in biological processes such as biological regulation and metabolic processes. Concerning cellular components, HJURP is primarily localized to the cell membrane and nucleus. In terms of molecular functions, it is chiefly enriched in activities related to protein binding and ion binding. HJURP was highly expressed in both clinical KIRC tissues and KIRC cell lines (P<0.001). In cultured KIRC cells, silencing of HJURP significantly inhibited cell proliferation and migration abilities. CONCLUSIONS HJURP may serves as an indicator of prognosis and immunotherapy response of KIRC, and its high expression enhances malignant behaviors of KIRC cells.
Humans ; Prognosis ; Kidney Neoplasms/pathology* ; Biomarkers, Tumor/metabolism* ; Carcinoma, Renal Cell/pathology* ; DNA-Binding Proteins/genetics* ; Cell Proliferation ; Cell Line, Tumor ; Cell Movement