Increased expression of CELSR3 indicates a poor prognostic factor for Prostate Cancer.

Cadherin EGF LAG Seven-Pass G-Type Receptor 3 (CELSR3) gene was reported to be overexpressed in various human cancers and involved in the regulation of neurite-dependent neurite outgrowth and may play a role in tumor formation. However, the clinical significance of CELSR3 in prostate cancer (PCa) has not been fully studied. The expression of CELSR3 was detected by crossover analysis of the public datasets and cell lines. MTT assay and migration assay were performed to evaluate the cells' physiological functioning. Co-expressed genes and enrichment analysis was performed to investigate the biological significance of CELSR3 in PCa. Quantitative real-time polymerase chain reaction was used to detect the expression levels of hub genes (CENPE, CENPA, CDC20, NUF2, ESPL1, PLK1) related to CELSR3. We found a significant increase in CELSR3 expression in PCa patients and cell lines. Furthermore, immunohistochemical analysis showed that CELSR3 protein expression was significantly more highly expressed in the PCa tissues compared to the non-cancerous PCa tissues. CELSR3 downregulation significantly suppressed cell proliferation and migration potential. CELSR3-related hub genes (CENPE, CENPA, CDC20, NUF2, ESPL1, PLK1) were selected and the functions of these hub genes showed that the function of CELSR3 was closely related to the cell cycle-related signaling pathways. The upregulation of CELSR3 mRNA expression in the PCa tissues significantly correlated with the presence of high serum PSA levels, high pathological stage, high Gleason score, short overall survival time and short disease-free survival time. Our data suggest that CELSR3 may play an important role in the progression of PCa. More importantly, an increase in CELSR3 expression may be indicative of poor disease-free survival and poor prognosis in PCa patients.