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GPR65 as a potential immune checkpoint regulates the immune microenvironment according to pan-cancer analysis
Liangliang Wang1, Lele Sun1, Hao Sun1
1Department of Forensic Medicine, Shanxi Medical University, Jinzhong, China.
Abstract:
It has been reported that inhibition of GPR65 may be effective for the treatment of certain cancers. Nevertheless, the role of GPR65 in various cancers remains unknown. We conducted an exhaustive pan-cancer analysis of GPR65 using multiple databases, including TCGA, GTEx, BioGPS, HPA, cBioPortal, and GeneCards. GPR65 was found to be differentially expressed in various cancers and linked to tumor mutational burden (TMB), microsatellite instability (MSI), and Ploidy, playing a key function in the tumor microenvironment (TME). It is closely linked to the development of Th17 cells as well as Th1 and Th2 cells in certain cancers. Our findings indicate that the expression of GPR65 is highly linked with clinical prognosis, mutations, and immune cell infiltration. It was revealed as an indicator of patient prognosis as well as a possible immunomodulatory role. As a possible new immunological checkpoint, GPR65 could be a target for tumor immunotherapy.
Insights
GPR65 (G protein-coupled receptor 65) shows varied expression across cancers, influencing tumor microenvironment and immune cells. This suggests GPR65 is a potential target for novel cancer immunotherapies.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Inhibiting GPR65 (G protein-coupled receptor 65) shows promise for cancer treatment.
- The specific role of GPR65 in diverse cancer types is not fully understood.
Purpose of the Study:
- To perform a comprehensive pan-cancer analysis of GPR65 expression and its functional relevance.
- To investigate the association of GPR65 with tumor characteristics and the tumor microenvironment (TME).
Main Methods:
- Utilized multiple public databases: TCGA, GTEx, BioGPS, HPA, cBioPortal, and GeneCards.
- Conducted an exhaustive pan-cancer analysis of GPR65 expression patterns and correlations.
Main Results:
- GPR65 exhibits differential expression in various cancers, impacting tumor mutational burden (TMB), microsatellite instability (MSI), and ploidy.
- GPR65 influences T-helper cell subsets (Th1, Th2, Th17) within the tumor microenvironment.
- GPR65 expression correlates significantly with clinical outcomes, genetic mutations, and immune cell infiltration.
Conclusions:
- GPR65 serves as a prognostic indicator in cancer patients.
- GPR65 possesses immunomodulatory functions and represents a potential target for cancer immunotherapy as a novel immune checkpoint.
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