ArticleCureus2025
Diagnostic, Prognostic, and Immunomodulatory Roles of Prostaglandin E Receptor 1 (PTGER1): A Pan-Cancer Study.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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.
resultsPTGER1 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.
conclusionAnalysis 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.