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The Pharmacogenomics "Side-effect" of TP53/EGFR in Non-small Cell Lung Cancer Accompanied with Atorvastatin Therapy:
Lei Zhang1, Yifang Huang1, Xuedong Gan2
1Center for Gene Diagnosis, Zhongnan Hospital of Wuhan University, Wuhan, China.
Background:
Atorvastatin belongs to the group of statins and is the leading drug for hypercholesterolemia treatment. Although, its anticancer effects are highly appreciated, its properties are still unclear. The aim of this study was to explore the underlying anticancer mechanisms induced by atorvastatin and enlarge the potential target in non-small cell lung cancer.
Methods:
Target genes of atorvastatin were collected by the DrugBank database. Prediction of interaction between primary targets and secondary targets was performed, and protein-protein interaction network was constructed though the STRING. Then, KEGG pathway enrichment analysis was performed with WebGestalt and ClueGO, including the pathways in non-small cell lung cancer. Furthermore, a genomic alteration analysis of the selected seed genes of atorvastatin benefit and non-small cell lung cancer pathway was conducted by cBioPortal. Finally, a survival analysis with the selected seed genes in lung cancer (lung adenocarcinoma, lung squamous cell carcinoma) was conducted using Kaplan-Meier (KM) plotter.
Results:
To identify seed genes, 65 potential candidate genes were screened as targets for atorvastatin using STRING with DrugBank database, while the KEGG pathway was enriched to get the overlap match of pathways in non-small cell lung cancer. Then 4 seed genes, Epidermal Growth Factor Receptor (EGFR), erb-b2 receptor tyrosine kinase 2 (ERBB2), AKT serine/threonine kinase 1 (AKT1) and tumor protein p53 (TP53), were selected and their genomic alternation were evaluated by cBioPortal. Survival analysis found that TP53 and EGFR showed a significant correlation (log rank P = 3e-07 and 0.023) with lung adenocarcinoma and lung squamous cell carcinoma, according to the KM analysis.
Conclusion:
Gene-phenotype connectivity for atorvastatin in non-small cell lung cancer was identified using functional/activity network analysis method, and our findings demonstrated that TP53 and EGFR could be the potential targets in cancer patients with atorvastatin therapy.
Insights
Atorvastatin, a cholesterol-lowering drug, shows potential anticancer effects in non-small cell lung cancer. TP53 and Epidermal Growth Factor Receptor (EGFR) were identified as key targets for atorvastatin therapy in lung cancer patients.
Area of Science:
- Oncology
- Pharmacology
- Bioinformatics
Background:
- Atorvastatin, a statin, is primarily used for hypercholesterolemia.
- Its anticancer properties are recognized but not fully understood.
- Non-small cell lung cancer (NSCLC) remains a significant health concern.
Purpose of the Study:
- To investigate the anticancer mechanisms of atorvastatin in NSCLC.
- To identify potential therapeutic targets for atorvastatin in NSCLC.
Main Methods:
- Utilized DrugBank and STRING for target gene identification and network construction.
- Performed KEGG pathway enrichment analysis using WebGestalt and ClueGO.
- Conducted genomic alteration analysis via cBioPortal and survival analysis using Kaplan-Meier plotter.
Main Results:
- Identified 4 key genes: Epidermal Growth Factor Receptor (EGFR), ERBB2, AKT1, and TP53.
- TP53 and EGFR demonstrated significant correlation with survival in lung adenocarcinoma and lung squamous cell carcinoma.
- Genomic alterations in these genes were evaluated.
Conclusions:
- Established gene-phenotype connectivity for atorvastatin in NSCLC.
- TP53 and EGFR are proposed as potential therapeutic targets for atorvastatin treatment in lung cancer patients.
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