Unveiling Lipid Metabolism-Related Gene PTGDS: A Tumor Suppressor in Lung Adenocarcinoma with Therapeutic Potential
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Published on: July 21, 2018
Boxuan Zhou1, Jianwei Shi1, Linchuan Liang1
1Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Chaoyang District, Panjiayuan, Nanli 17, Beijing 100021, China.
Background:
Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Although the lipid metabolism-associated gene PTGDS has been implicated in tumorigenesis, its functional significance and regulatory mechanisms in LUAD are poorly understood.
Methods:
We integrated multi-omics data from TCGA and GEO cohorts to evaluate PTGDS expression and its clinicopathological relevance. Functional characterization was performed using gain-of-function models in LUAD cell lines and a xenograft mouse model, assessing proliferation, migration, invasion, and immune microenvironment alterations.
Results:
PTGDS expression is markedly reduced in LUAD tissues and correlates strongly with advanced disease stage and unfavorable prognosis. Clinically, low PTGDS expression is associated with specific driver mutations and reduced tumor mutation burden. Notably, PTGDS levels correlate with enhanced cytotoxic T-cell infiltration and suppressed M2 macrophage polarization, suggesting immunomodulatory functions. Ectopic expression of PTGDS significantly suppressed malignant behaviors in vitro and tumor growth in vivo. Mechanistically, PTGDS overexpression was associated with reduced expression of CDK1 and PLK1 and increased expression of p21 and p27.
Conclusions:
Our findings establish PTGDS as a novel tumor suppressor in LUAD that restrains tumor progression through cell cycle modulation and immune microenvironment remodeling, highlighting its potential as both a prognostic biomarker and a therapeutic target.
Insights
Prostaglandin D synthase (PTGDS) acts as a tumor suppressor in lung adenocarcinoma (LUAD). Reduced PTGDS restrains LUAD progression by modulating cell cycle and the immune microenvironment, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Lung adenocarcinoma (LUAD) is a major cause of cancer mortality.
- The role of the lipid metabolism gene PTGDS in LUAD tumorigenesis is unclear.
Purpose of the Study:
- To investigate the function and regulation of PTGDS in LUAD.
- To evaluate PTGDS as a prognostic biomarker and therapeutic target in LUAD.
Main Methods:
- Integrated multi-omics data from TCGA and GEO cohorts.
- Utilized LUAD cell line and xenograft mouse models for functional characterization.
- Assessed proliferation, migration, invasion, and immune microenvironment alterations.
Main Results:
- PTGDS expression is decreased in LUAD and linked to advanced stage and poor prognosis.
- Low PTGDS correlates with specific mutations and reduced tumor mutation burden.
- PTGDS influences cytotoxic T-cell infiltration and M2 macrophage polarization, suppressing tumor growth and malignant behaviors via cell cycle regulators.
Conclusions:
- PTGDS functions as a tumor suppressor in LUAD.
- PTGDS restrains LUAD progression by modulating cell cycle and immune microenvironment.
- PTGDS shows potential as a prognostic biomarker and therapeutic target for LUAD.
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