# PTGDS is a potential marker for lung adenocarcinoma identified in a pancancer analysis

## TL;DR

This study finds that PTGDS is a potential marker for lung adenocarcinoma and plays a role in cancer progression and immunity across various tumor types.

## Contribution

The study identifies PTGDS as a tumor suppressor in lung adenocarcinoma and explores its pancancer implications.

## Key findings

- PTGDS is dysregulated across various cancers and correlates with patient survival.
- PTGDS influences tumor immunity and is associated with immune cell types like natural killer cells and macrophages.
- PTGDS inhibits lung adenocarcinoma cell proliferation through fatty acid degradation and cell cycle regulation.

## Abstract

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).

The online version contains supplementary material available at 10.1038/s41598-026-38688-0.