Journal of cancer research and therapeutics
May 27, 2026 · via Europe PMC
Association between lipid metabolism and lung adenocarcinoma: Evidence from Mendelian randomization and tissue microbiome analysis.
Chen Q, Xu Z, Zheng T, Pang H, He Z.
AI summary — for doctors, generated from the abstract only
Mendelian randomization suggested saturated fatty acids and cholesterol increase and linoleic acid decreases lung adenocarcinoma risk, and tissue microbiome and gene analyses highlighted GPLD1 as a candidate biomarker.
What was studied
Mendelian randomization of lipid traits with LUAD, plus TCGA/GEO tumor microbiome and gene expression analyses and qPCR validation.
Key findings
- Saturated fatty acids and total cholesterol identified as risk factors; linoleic acid protective
- Bacillus velezensis enriched in LUAD tissue
- Twelve cholesterol-related genes formed a prognostic risk model
- GPLD1 lower in tumors and plasma of lung cancer patients, linked to worse survival
Clinical relevance
This exploratory work generates hypotheses about diet, microbiome and lung cancer; it has no immediate clinical application.
Who should care
Limitations
MR assumptions and bioinformatic analyses require validation.
Dietary fats may influence lung adenocarcinoma risk, and GPLD1 is a candidate blood marker.
This is an AI-generated summary of the published abstract, not a clinical recommendation. It may not reflect the full text or subsequent updates — verify against the original source before acting on it.
Abstract
Background
Tissue-resident microbiota play an important role in lung cancer development. This study aimed to characterize the microbiota profile associated with fatty acid metabolism and related genes and examine its effect on treatment outcomes in lung cancer.
Methods
Genome-wide association data on saturated fatty acid ratio, total cholesterol, and linoleic acid ratio were analyzed with lung adenocarcinoma as the outcome. Mendelian randomization (MR) and multivariable MR using significant single nucleotide polymorphisms assessed causal effects with sensitivity analyses. TCGA and GEO microbial data were explored via GSEA, STRING, and CIBERSORT, and Bacillus velezensis was validated in tumor tissue by quantitative polymerase chain reaction.
Results
MR identified saturated fatty acids and total cholesterol as risk factors for lung adenocarcinoma (LUAD), while linoleic acid was protective. Microbial profiling showed distinct tumor versus adjacent tissue communities, with Bacillus velezensis enriched in LUAD. Its abundance was negatively associated with the cholesterol-response pathway (GOBP_CELLULAR_RESPONSE_TO_CHOLESTEROL). Twelve cholesterol-related genes were differentially expressed, and a derived risk model predicted poor prognosis. Among them, GPLD1 exhibited tumor-suppressor characteristics, with lower tumor expression linked to worse survival. GPLD1 is detectable in plasma (~2.8 mg/L) and reduced in lung cancer patients, supporting its potential as a noninvasive biomarker.
Conclusion
Our findings suggest a causal link between the components of a high-fat diet and LUAD by identifying key genes and microbial communities. Moreover, GPLD1 represents a promising biomarker for the early diagnosis and prognosis of this patient population.
DOI
10.4103/jcrt.jcrt_2333_25
PMID
42241172
Research metadata (titles, abstracts, authors, publication dates) is sourced from Europe PMC, which aggregates content from PubMed/MEDLINE, PubMed Central, and other providers under the U.S. National Library of Medicine (NLM/NCBI). NLM does not claim copyright on abstracts; the original journal publishers or authors may hold rights to the full articles. AI-generated summaries are derived only from the abstract, never the full text, and are always labeled as AI-generated.
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