RETRACTED: S1P3 promotes low-grade glioma progression and affects tumor microenvironment infiltration

Abstract

Numerous human tumors have been demonstrated to develop in a manner that is correlated with the S1P/S1P3 axis. However, it is yet unclear how this axis could affect the development of glioma, specifically TME cell invasion. We examined the clinicopathological data and gene expression data of gliomas to evaluate overall survival using univariate and multivariate Cox regression. By using Gene Set Enrichment Analysis, we investigated the signaling pathways and genes linked to S1P3 overexpression. We also examined the traits of biological pathways, TME immune cell infiltration, and oncogenic pathways (OP) in glioma samples with different S1P3 expression levels, and we validated the findings using PCR, CCK8, and wound healing assays. S1P3 overexpression was substantially linked with molecular typing and overall survival, according to Cox regression analysis. The Nomogram for predicting prognosis was successfully constructed by using S1P3 and other molecular signatures of gliomas, and Gene Set Enrichment Analysis revealed the relationship between S1P3 overexpression and DNA replication, cell cycle, MAPK, p53 and TGF-β signaling pathways. In addition, S1P3 was significantly correlated with many immune checkpoints and immune cell infiltration. Overall, S1P3 overexpression is a potential prognostic molecular marker for poor prognosis in glioma. Additionally, S1P3 acts as an important player in TME immune cell infiltration. The identification of S1P3-regulated signaling pathways and immune checkpoints strengthens our understanding of TME infiltration signatures and contributes to the development of immunotherapeutic strategies.