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Bioinformatic Analysis for Exploring Target Genes and Molecular Mechanisms of Cadmium-Induced Nonalcoholic Fatty
Le Zhang1, Rui Wang1, Qian Xue1
1Department of Toxicology, School of Public Health, Jilin University, Changchun, China.
Abstract:
Cadmium (Cd) is a widely available metal that has been found to have a role in causing nonalcoholic fatty liver disease (NAFLD). However, the detailed toxicological targets and mechanisms by which Cd causes NAFLD are unknown. Therefore, the present work aims to reveal the main targets of action, cellular processes, and molecular pathways by which cadmium causes NAFLD. As shown in the bioinformatics analysis, there were 74 main targets of action for cadmium-induced NAFLD, hemopoietic cell kinase (HCK), EPH receptor A2 (EPHA2), MYC proto-oncogene (MYC), lysyl oxidase (LOX), dipeptidyl peptidase 7 (DPP7), nuclear factor erythroid 2-related factor 2 (NFE2L2), dual specificity phosphatase 6 (DUSP6), CD2 cytoplasmic tail binding protein 2 (CD2BP2), notch receptor 3 (NOTCH3), and phospholipase A2 group IVA (PLA2G4A) were screened as core genes. Testing these core genes in other databases, three differentially expressed genes, HCK, MYC, and DUSP6 were verified and used as targets for drug prediction in DsigDB; decitabine and retinoic acid were screened as potential therapeutic drugs for NAFLD based on the p-value and the combined score. The results of molecular docking showed that the predicted drugs can bind well to the core targets. In conclusion, cadmium is associated with NAFLD; the identified cadmium-toxicity targets, HCK, MYC, and DUSP6, may serve as biomarkers for the diagnosis of NAFLD and predicted drugs, decitabine and retinoic acid may have a potential role in the treatment of NAFLD.
Insights
Cadmium exposure is linked to nonalcoholic fatty liver disease (NAFLD). Researchers identified key genes (HCK, MYC, DUSP6) involved in cadmium toxicity and proposed decitabine and retinoic acid as potential treatments for NAFLD.
Area of Science:
- Toxicology
- Bioinformatics
- Hepatology
Background:
- Cadmium (Cd) is a prevalent environmental metal.
- Cd exposure is associated with nonalcoholic fatty liver disease (NAFLD).
- The precise mechanisms of Cd-induced NAFLD remain unclear.
Purpose of the Study:
- To elucidate the primary molecular targets, cellular processes, and pathways involved in Cd-induced NAFLD.
- To identify potential biomarkers for NAFLD diagnosis.
- To discover novel therapeutic agents for NAFLD treatment.
Main Methods:
- Bioinformatic analysis to identify 74 Cd-NAFLD targets.
- Screening of core genes including hemopoietic cell kinase (HCK), MYC proto-oncogene (MYC), and dual specificity phosphatase 6 (DUSP6).
- Drug prediction using DsigDB and molecular docking to validate drug-target interactions.
Main Results:
- Bioinformatics identified 74 Cd-NAFLD targets, with HCK, MYC, and DUSP6 confirmed as core genes.
- Decitabine and retinoic acid were identified as potential therapeutic drugs for NAFLD.
- Molecular docking confirmed favorable binding of the predicted drugs to the core targets.
Conclusions:
- Cadmium exposure is significantly associated with NAFLD.
- HCK, MYC, and DUSP6 are identified as potential biomarkers for NAFLD diagnosis.
- Decitabine and retinoic acid show promise as therapeutic agents for treating NAFLD.
