CDCA7: A Comprehensive Pan-Cancer Analysis Reveals its Prognostic Significance, Immune Correlations, and Therapeutic Potential

Abstract

Background Recent years have witnessed the emergence of Cell Division Cycle Associated 7 (CDCA7) as a participant in the genesis of diverse tumors. Despite this, comprehensive pan-cancer evaluations of CDCA7 remain scarce. Consequently, this study aims to rectify this gap by scrutinizing the potential implications of CDCA7 in pan-cancers. Methods We first assessed the expression levels of CDCA7 in 33 cancers and the association of its expression with tumor pathological stage using TCGA, GTEx, GEPIA2, TIMER2.0, TISIDB, UALCAN, and StarBase. Then, prognostic assessment was performed using GEPIA2 and Kaplan-Meier plotter. Gene alterations of CDCA7 were analyzed using cBioPortal, and renal clear cell carcinoma cells lines were screened to determine the function of CDCA7. Finally, we performed tumor immune infiltration analysis using TIMER2.0 and enrichment analysis of CDCA7 by STRING, GEPIA2, and DAVID. The role of CDCA7 in renal clear cell carcinoma (cc) was verified by qPCR, CCK8, wound healing, transwell and cell cycle assay. Results Our study demonstrated that CDCA7 exhibited notable expression across various cancers, and its heightened expression correlated with an unfavorable prognosis for tumor patients. Correlations emerged between CDCA7 expression and the presence of tumor-infiltrating immune cells (TIICs). Moreover, CDCA7 upregulation corresponded to CD8+ T cell infiltration in some tumors. Most malignancies demonstrated a positive relationship between CDCA7 and cancer-associated fibroblast infiltration. Enrichment studies unveiled CDCA7's involvement in cell cycle and DNA metabolism, in addition to its role in multiple signaling pathways that drive tumor progression. Experimental validations underscored CDCA7's role in stimulating the progression of renal clear cell carcinoma. Insights from CCK8 and cell cycle assays confirmed that CDCA7 inhibition attenuated cellular activity and curtailed proliferative capacity in 769-P cells. Wound healing and Transwell assays substantiated that CDCA7 blockade significantly reduced migration and invasion capabilities of 769-P cells. Additionally, quantitative PCR results corroborated the efficacy of CDCA7 inhibition in preventing the epithelial-mesenchymal transition state of renal clear cell carcinoma. Conclusions In conclusion, the comprehensive pan-cancer investigation imparts intricate insights into the engagement of CDCA7 in carcinogenesis. Our findings indicate that CDCA7 holds the potential to serve as a valuable prognostic marker and an alluring target for therapeutic interventions, thereby unveiling novel avenues for future research.