Knockdown of HJURP inhibits non-small cell lung cancer cell proliferation, migration, and invasion by repressing Wnt/β-catenin signaling.

Holliday junction-recognizing protein (HJURP) was found to be upregulated in several tumors, including non-small cell lung cancer (NSCLC), and the effect of HJURP on NSCLC remains unknown. The objective of the present study was to explore the clinical significance of HJURP and its function in regulating the progression of NSCLC. Reverse Transcriptions-Polymerase Chain Reaction (RT-PC) and Western blot were performed to detect the expression levels of HJURP in NSCLC tissues and cell lines. The association of HJURP expression level with various important clinicopathological parameters was evaluated. Then, the effects of HJURP expression on tumor cell behavior in vitro were analyzed by the Cell Counting Kit-8 (CCK-8), EdU assays, colony formation, flow cytometry, and transwell assays. The protein levels of related proteins of the Wnt/β-catenin pathway were determined using the Western blot assay. Our study showed that HJURP was significantly upregulated in both NSCLC tissues and cell lines. The higher expression of HJURP was associated with advanced TNM stage, distant metastasis, and poor prognosis. Our data from in vitro assays confirmed that the knockdown of HJURP suppressed NSCLC cells proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) progress, and induced cells apoptosis. Notably, through Western blot analysis, we found that HJURP suppression remarkably decreased β-catenin, cyclin D1 and c-myc expression level in NSCLC cell lines. Our findings provide clues regarding the role of HJURP as a tumor promoter in NSCLC via the activation of the Wnt/β-catenin pathway, indicating HJURP may be a promising therapeutic target for NSCLC.