Genetically predicted inflammatory protein mediate the association between lipidome and colon cancer
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View abstract on PubMed
Summary
This summary is machine-generated.This study used Mendelian randomization to find causal links between seven lipidome levels and colon cancer risk. Some effects were mediated by inflammatory factors like TNF-related apoptosis-inducing ligand.
Area Of Science
- Genetics
- Metabolomics
- Oncology
Background
- Dyslipidemia and inflammatory proteins are correlated with colon cancer, but causal links remain unclear.
- A comprehensive analysis is needed to establish causality between lipid metabolism and colon cancer.
Purpose Of The Study
- To investigate the potential causal relationships between various lipidome levels and colon cancer risk.
- To explore the mediating role of inflammatory factors in the lipidome-colon cancer association.
Main Methods
- A two-sample Mendelian Randomization (MR) strategy was employed.
- Bayesian Weighted Mendelian Randomization (BWMR) and MR-robust adjusted profile score (MR-RAPS) were used for validation.
- Inverse MR analysis and mediation analysis were performed to assess reverse causation and inflammatory mediation.
Main Results
- Seven specific lipidome levels showed potential causal correlations with colon cancer risk.
- Negative correlations were observed for Phosphatidylcholine (O-16:1_18:0), Phosphatidylethanolamine (O-16:1_22:5), and Phosphatidylethanolamine (O-18:1_18:2).
- Positive correlations were found for Sterol ester (27:1/18:3), Phosphatidylcholine (18:0_22:5), Triacylglycerol (46:1), and Triacylglycerol (46:2).
- Tumor Necrosis Factor (TNF)-related apoptosis-inducing ligand mediated some effects of Phosphatidylcholine (18:0_22:5) and Phosphatidylethanolamine (O-16:1_22:5) on colon cancer.
Conclusions
- Mendelian randomization analysis supports potential causal links between seven lipidome profiles and colon cancer.
- Inflammatory factors, such as TNF-related apoptosis-inducing ligand, play a mediating role in these associations.
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