A Comprehensive Prognostic Analysis of Slit2 in Pan-Cancer
Background: Previous studies have partly explored the role of axon guidance protein family member slit guidance ligand 2(Slit2) in tumorigenesis and development.However,the expression of Slit2 in pan-cancer still unclear.In this paper, we firstly study the expression of Slit2 in pan-cancer and the performance of prognosis, clinical features, immunity, etc. Methods: Data were obtained from the Cancer Genome Atlas (TCGA), the Genotype-Tissue Expression (GTEx) databases, and the University of California Santa Cruz (UCSC) Xena.We analyzed the expression of the Slit2 gene in 33 tumors and adjacent normal tissues, using TCGA_GTEx samples, TCGA samples, and paired samples from the TCGA database.Next, we employed the Kaplan-Meier method, including univariate Cox regression analysis and Kaplan-Meier curves to identify 33 tumors in which Slit2 gene expression correlates with prognosis, as per clinical analysis.For cancers like bladder urothelial carcinoma (BLCA) and colon adenocarcinoma (COAD), we constructed nomogram models to validate the prognostic significance of Slit2 in cancer.Subsequently, we analyzed the association of Slit2 with immune cell infiltration.Furthermore, we utilized the receiver operating characteristic (ROC) curve to assess the diagnostic value of the Slit2 gene.Participated in and conducted functional enrichment analysis to investigate potential signaling pathways associated with Slit2.Results: Our study reveals that Slit2 is differentially expressed in various tumors and correlates with clinical outcomes and the immune microenvironment.The result suggests that Slit2 may influence the tumor development and progression through diverse pathways.Conclusion: In summary, Slit2 may be a potential prognostic biomarker in pan-cancer.
Authors
- Dongliang Guo
Publication Details
- Journal
- Research Review
- Published
- 2025-08-04
- DOI
- https://doi.org/10.52845/cs/2025-5-3-83
- Primary Topic
- Axon Guidance and Neuronal Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00