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Identification of key genes and pathways and therapeutic agents in cadmium-treated liver cells: A bioinformatics
Liang Zhang1, Yi Huang2, Zhen Yu3
1College of Food Science and Nutritional Engineering, China Agriculture University, Beijing, China; Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China.
Abstract:
Evidence indicates that Cadmium (Cd) can accumulate in liver, which results in acute or chronic cell damage with unclear complex mechanisms. Thus, we aimed to explore the possible molecules and pathways by using bioinformatics methods Consequently, two datasets (GSE8865 and GSE31286) were retrieved and the differentially expressed genes (DEGs) were screened out. The intersection of the DEGs included seven up-regulated and forty-three down-regulated genes, which were mainly enriched in biological cell proliferation items, and were enriched in several metabolism-related pathways. Among the DEGs, several hub genes such as EGR1, FOSL1, ITGA2, EDN1, and IER3 were screened out through protein-protein interaction analysis. Interestingly, BW-B70C was predicted to be a potential agent for attenuating Cd-induced liver cell damage. The present study gave a novel insight into the mechanisms of Cd-induced liver cell damage or malignant transformation and identified several small agents that might be critical for Cd toxicity prevention and treatment.
Insights
Cadmium (Cd) exposure causes liver cell damage through complex mechanisms. This study identified key genes and pathways involved, offering potential therapeutic targets for Cd toxicity.
Area of Science:
- Hepatology
- Toxicology
- Bioinformatics
Background:
- Cadmium (Cd) accumulates in the liver, causing cell damage via complex, not fully understood mechanisms.
- Investigating molecular pathways is crucial for understanding and mitigating Cd-induced liver injury.
Purpose of the Study:
- To explore the molecular mechanisms and pathways underlying Cadmium-induced liver cell damage using bioinformatics.
- To identify potential therapeutic agents for Cadmium toxicity.
Main Methods:
- Differential gene expression analysis of two public datasets (GSE8865 and GSE31286).
- Protein-protein interaction network analysis to identify hub genes.
- Pathway and gene ontology enrichment analysis.
Main Results:
- Identified 7 up-regulated and 43 down-regulated differentially expressed genes (DEGs) in response to Cadmium.
- DEGs were significantly enriched in cell proliferation and metabolism-related pathways.
- Key hub genes (e.g., EGR1, FOSL1, ITGA2, EDN1, IER3) were identified.
- BW-B70C was predicted as a potential agent to reduce Cadmium-induced liver damage.
Conclusions:
- This study provides novel insights into the mechanisms of Cadmium-induced liver damage and potential malignant transformation.
- Identified key genes and pathways offer targets for preventing and treating Cadmium toxicity.
- BW-B70C shows promise as a therapeutic agent for Cadmium-induced liver injury.