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Published on: March 14, 2019
Identification and analysis of the molecular targets of statins in colorectal cancer
Ali Ahmadizad Firouzjaei1, Ali Mahmoudi2, Wael Almahmeed3
1Student Research Committee, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran; Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Colorectal cancer (CRC) is the third most common cancer in the world. According to several types of research, statins may impact the development and treatment of CRC. This work aimed to use bioinformatics to discover the relationship between statin targets and differentially expressed genes (DEGs) in CRC patients and determine the possible molecular effect of statins on CRC suppression. We used CRC datasets from the GEO database to select CRC-related DEGs. DGIdb and STITCH databases were used to identify gene targets of subtypes of statin. Further, we identified the statin target of CRC DEGs hub genes by using a Venn diagram of CRC DEGs and statin targets. Funrich and enrichr databases were carried out for the KEGG pathway and gene ontology (GO) enrichment analysis, respectively. GSE74604 and GSE10950 were used to identify CRC DEGs. After analyzing datasets,1370 genes were identified as CRC DEGs, and 345 targets were found for statins. We found that 35 genes are CRC DEGs statin targets. We found that statin targets in CRC were enriched in the receptor and metallopeptidase activity for molecular function, cytoplasm and plasma membrane for cellular component, signal transduction, and cell communication for biological process genes were substantially enriched based on FunRich enrichment. Analysis of the KEGG pathways revealed that the overexpressed DEGs were enriched in the IL-17, PPAR, and Toll-like receptor signaling pathways. Finally, CCNB1, DNMT1, AURKB, RAC1, PPARGC1A, CDKN1A, CAV1, IL1B, and HSPD1 were identified as hub CRC DEGs statin targets. The genetic and molecular aspects of our findings reveal that statins might have a therapeutic effect on CRC.
Insights
Statins may help suppress colorectal cancer (CRC) by targeting specific genes. This bioinformatics study identified 35 overlapping genes between statin targets and CRC differentially expressed genes (DEGs), suggesting a potential therapeutic role for statins in CRC treatment.
Area of Science:
- Oncology
- Bioinformatics
- Pharmacology
Background:
- Colorectal cancer (CRC) is a major global health concern.
- Statins, commonly used for cholesterol management, are being investigated for their potential role in CRC development and treatment.
- Understanding the molecular interplay between statins and CRC is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the relationship between statin targets and differentially expressed genes (DEGs) in colorectal cancer (CRC) using bioinformatics.
- To identify potential molecular mechanisms by which statins may suppress CRC progression.
- To discover key overlapping genes (hub genes) between statin targets and CRC DEGs.
Main Methods:
- Utilized CRC gene expression datasets from the GEO database to identify DEGs.
- Employed DGIdb and STITCH databases to identify statin gene targets.
- Applied Venn diagrams to find overlapping genes between CRC DEGs and statin targets.
- Conducted KEGG pathway and Gene Ontology (GO) enrichment analyses using Funrich and Enrichr databases.
Main Results:
- Identified 1370 CRC DEGs and 345 statin targets, with 35 overlapping genes.
- Enrichment analysis revealed statin targets in CRC are associated with receptor activity, metallopeptidase activity, signal transduction, and cell communication.
- KEGG pathway analysis highlighted enrichment in IL-17, PPAR, and Toll-like receptor signaling pathways.
- Identified hub genes including CCNB1, DNMT1, AURKB, RAC1, PPARGC1A, CDKN1A, CAV1, IL1B, and HSPD1.
Conclusions:
- Bioinformatic analysis reveals a significant overlap between statin targets and DEGs in colorectal cancer.
- Statin targets in CRC are implicated in key molecular functions and signaling pathways relevant to cancer progression.
- The identified hub genes and enriched pathways suggest that statins possess therapeutic potential for CRC, warranting further investigation.
