Cureus · 2025
Diagnostic, Prognostic, and Immunomodulatory Roles of Prostaglandin E Receptor 1 (PTGER1): A Pan-Cancer Study.
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Suliman Rasha, Alfaki Mohamed
Аннотация
BACKGROUND: The prostaglandin E receptor 1 (PTGER1) is a G-protein-coupled receptor (GPCR) located on chromosome 9. It encodes prostaglandin E2 receptor 1 (EP1), a 42kDa prostaglandin receptor involved in mediating many physiological and pathological responses to prostaglandin E2 (PGE2), including inflammation, pain perception, and modulation of cell proliferation. We performed a pan-cancer, multi-omics analysis of PTGER1 to evaluate its diagnostic, prognostic, and immunological relevance across human cancers.
METHODOLOGY: We used multiple public cancer bioinformatics platforms including the Tumor Immune Estimation Resource (TIMER), Gene Expression Profiling Interactive Analysis (GEPIA), and the University of ALabama at Birmingham CANcer Data Analysis Portal (UALCAN), Kaplan-Meier (KM-Plotter), CbioPortal and Gene Expression Omnibus (GEO) to evaluate PTGER1 expression, methylation, immune infiltration, genetic alteration and survival across tumor types.
RESULTS: PTGER1 revealed significant (P < 0.05) expression in four cancer types; it was downregulated in kidney chromophobe (KICH) and kidney renal cell carcinoma (KIRC), uterine corpus endometrial cancer (UCEC), and upregulated in liver hepatocellular carcinoma (LIHC). Moreover, a significant hypermethylation of normal cells was noted in bladder carcinoma (BLCA), KIRC, and lung adenocarcinoma (LUAD). A significant hypermethylation of tumor cells in UCEC and kidney renal papillary (KIRP), and head and neck squamous carcinoma (HNSC) was noted. Interestingly, KICH showed staged methylation. PTGER1 demonstrated a statistically significant (P < 0.05), weakly positive correlation with immune cell populations, including CD8⁺ T cells, CD4⁺ T cells, dendritic cells, B cells, neutrophils, and macrophages in KIRC, KICH, and LIHC. Subsequently, prognostic analysis indicated that elevated PTGER1 expression was associated with poorer outcomes in KIRC and lung squamous cell carcinoma (LUSC) across three databases and improved prognosis in LIHC. From a genomic perspective, across a variety of cancers, PTGER1 was altered in approximately <2% (160 samples out of 10960 samples) primarily through gene amplification.
CONCLUSION: Analysis and cross-referencing across three publicly available databases revealed that PTGER1 is promising as a diagnostic biomarker in KICH and KIRC and a poor prognostic biomarker in KIRC and LUSC.
METHODOLOGY: We used multiple public cancer bioinformatics platforms including the Tumor Immune Estimation Resource (TIMER), Gene Expression Profiling Interactive Analysis (GEPIA), and the University of ALabama at Birmingham CANcer Data Analysis Portal (UALCAN), Kaplan-Meier (KM-Plotter), CbioPortal and Gene Expression Omnibus (GEO) to evaluate PTGER1 expression, methylation, immune infiltration, genetic alteration and survival across tumor types.
RESULTS: PTGER1 revealed significant (P < 0.05) expression in four cancer types; it was downregulated in kidney chromophobe (KICH) and kidney renal cell carcinoma (KIRC), uterine corpus endometrial cancer (UCEC), and upregulated in liver hepatocellular carcinoma (LIHC). Moreover, a significant hypermethylation of normal cells was noted in bladder carcinoma (BLCA), KIRC, and lung adenocarcinoma (LUAD). A significant hypermethylation of tumor cells in UCEC and kidney renal papillary (KIRP), and head and neck squamous carcinoma (HNSC) was noted. Interestingly, KICH showed staged methylation. PTGER1 demonstrated a statistically significant (P < 0.05), weakly positive correlation with immune cell populations, including CD8⁺ T cells, CD4⁺ T cells, dendritic cells, B cells, neutrophils, and macrophages in KIRC, KICH, and LIHC. Subsequently, prognostic analysis indicated that elevated PTGER1 expression was associated with poorer outcomes in KIRC and lung squamous cell carcinoma (LUSC) across three databases and improved prognosis in LIHC. From a genomic perspective, across a variety of cancers, PTGER1 was altered in approximately <2% (160 samples out of 10960 samples) primarily through gene amplification.
CONCLUSION: Analysis and cross-referencing across three publicly available databases revealed that PTGER1 is promising as a diagnostic biomarker in KICH and KIRC and a poor prognostic biomarker in KIRC and LUSC.