PTGDS is a potential marker for lung adenocarcinoma identified in a pancancer analysis - Predictive role, prognosis, and immune regulation

Sep 22, 2026

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Prostaglandin D2 synthase (PTGDS) is investigated as a broad cancer biomarker using multiomics integration. Results show widespread dysregulation of PTGDS across cancers and associations with patient survival. PTGDS correlates with stem cell and microenvironment scores, MSI status, tumor mutational burden, and methylation patterns, alongside immune correlations supported by single-cell transcriptomic data. Functional experiments demonstrate PTGDS inhibits lung adenocarcinoma cell proliferation via fatty acid degradation and cell-cycle regulation, supporting a tumor-suppressive prognostic role in LUAD.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages16

Reading Time40 min

AccessFree to download

Background and rationale

PTGDS biology and prior cancer links

Tumor immune microenvironment and multiomics profiling

Study objectives and datasets

PTGDS across 33 cancer types

Lung adenocarcinoma single-cell deep dive and validation

Results overview

PTGDS expression and protein levels across cancers

[www. nature.com/scientificreports](www. nature.com/scientificreports) OPEN PTGDS is a potential marker for lung adenocarcinoma identified ina pancancer analysis Runzhi Wang1,5, Fengling Shao2,5, Deng Liu4, Jun Chen3􀀍 & Qin Zhou4􀀍 Prostaglandin D2 synthase (PTGDS) is the enzyme responsible for synthesizing prostaglandin D2 . Despite its crucial role, PTGDS remains relatively understudied in tumor therapy, and comprehensive pancancer analyses are lacking. By leveraging multiomics data integration, this study elucidated the widespread dysregulation of PTGDS across various cancers and its correlation with patient survival. Moreover, PTGDS is significantly associated with stem cell scores, microenvironmental scores, microsatellite instability (MSI) status, tumor mutational burden (TMB), and methylation status in diverse tumor types. Additionally, immune correlations with PTGDS are evident across most cancers, with single-cell transcriptome data indicating predominant associations with natural killer cells and macrophages. Notably, experimental validation revealed the role of PTGDS in inhibiting A549 and H1975 lung adenocarcinoma cell proliferation, which was mediated by fatty acid degradation and cell cycle regulation. In summary, PTGDS has prognostic potential, influences pancancer tumor immunity, and acts as a tumor suppressor in lung adenocarcinoma (LUAD) . Keywords PTGDS, LUAD, TCGA, Pan-cancer PTGDS (prostaglandin D2 synthase) was initially classified within the lipocalin family and is located in the HSA9q34 region of the human genome1. Consequently, early investigations focused primarily on prostaglandin D2 (PGD2), which is derived from prostaglandin H2 (PGH2) via PTGDS catalysis2,3. Concurrently, genetic variations in PTGDS have been observed across various nonneoplastic diseases4–6. Recent studies have increasingly underscored the pivotal role of PTGDS in cancer. For example, PTGDS was found to promote diffuse large B-cell lymphoma tumorigenesis by regulating the MYH9-mediated Wnt β–catenin STAT3 signaling pathway7. Additionally, its downregulation by miRNA-155 leads to prostaglandin reprogramming in breast cancer8. PTGDS has also been implicated in counteracting the tumor-promoting effects of YAP in gastric cancer, inhibiting the proliferation and migration of breast cancer cells9, 10, and participating in the progression of cervical squamous cell carcinoma along with SNX1011. The tumor immune microenvironment (TME) critically influences cancer progression and the therapeutic response. Recent advances in multiomics analysis, exemplified by tools such as the iMLGAM platform12, have demonstrated how comprehensive TME profiling can predict immunotherapy outcomes by evaluating immune cell infiltration patterns. Notably, such approaches have identified key regulators, such as CEP55, that modulate T-cell responses, paralleling our interest in the potential immune regulatory functions of PTGDS. Despite these insights, the comprehensive assessment of PTGDS gene expression in tumorigenesis and its prognostic implications across various cancer types remains unexplored. The advancement of next-generation sequencing (NGS) in recent years has revolutionized clinical cancer management13. Notably, data acquired through initiatives such as The Cancer Genome Atlas (TCGA) project have fueled cross-tumor research endeavors14. These efforts aim to identify novel prognostic molecules and therapeutic targets via multiomics analysis (including whole transcriptomics, proteomics, and single-cell transcriptomics) of tumor specimens from diverse cancer cohorts15, 16. For example, leveraging TCGA data, researchers have probed the association between LRRC4C and the tumor immune microenvironment in colon and gastric cancers, alongside its clinical prognostic relevance17. Bai et al. investigated the prognostic 1The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150000, P. R. China. 2The Ministry of Education Key Labor

FAQs

What question does the study address about PTGDS in cancer?

The study evaluates whether PTGDS is broadly dysregulated across cancers, linked to patient outcomes, and functionally involved in tumor biology, with emphasis on lung adenocarcinoma.

Which clinical and molecular features correlate with PTGDS?

PTGDS is reported to associate with stem cell and microenvironment scores, MSI status, tumor mutational burden, and methylation patterns across diverse tumor types.

How was PTGDS validated in lung adenocarcinoma, and what mechanism was proposed?

Experimental validation shows PTGDS inhibits A549 and H1975 LUAD cell proliferation, mediated by fatty acid degradation and cell-cycle regulation.

Sep 22, 2026

Upload by Riley