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The underlying molecular mechanism and potential drugs for treatment in papillary renal cell carcinoma: A study based
Jin-Shu Pang1, Zhe-Kun Li1, Peng Lin2
1Department of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Abstract:
Papillary renal cell carcinoma (PRCC) accounts for 15‑20% of all kidney neoplasms and continually attracts attention due to the increase in the incidents in which it occurs. The molecular mechanism of PRCC remains unclear and the efficacy of drugs that treat PRCC lacks sufficient evidence in clinical trials. Therefore, it is necessary to investigate the underlying mechanism in the development of PRCC and identify additional potential anti‑PRCC drugs for its treatment. The differently expressed genes (DEGs) of PRCC were identified, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses for functional annotation. Then, potential drugs for PRCC treatment were predicted by Connectivity Map (Cmap) based on DEGs. Furthermore, the latent function of query drugs in PRCC was explored by integrating drug‑target, drug‑pathway and drug‑protein interactions. In total, 627 genes were screened as DEGs, and these DEGs were annotated using KEGG pathway analyses and were clearly associated with the complement and coagulation cascades, amongst others. Then, 60 candidate drugs, as predicted based on DEGs, were obtained from the Cmap database. Vorinostat was considered as the most promising drug for detailed discussion. Following protein‑protein interaction (PPI) analysis and molecular docking, vorinostat was observed to interact with C3 and ANXN1 proteins, which are the upregulated hub genes and may serve as oncologic therapeutic targets in PRCC. Among the top 20 metabolic pathways, several significant pathways, such as complement and coagulation cascades and cell adhesion molecules, may greatly contribute to the development and progression of PRCC. Following the performance of the PPI network and molecular docking tests, vorinostat exhibited a considerable and promising application in PRCC treatment by targeting C3 and ANXN1.
Insights
This study identifies key genes and pathways involved in papillary renal cell carcinoma (PRCC) and predicts vorinostat as a promising drug for PRCC treatment by targeting C3 and ANXN1 proteins.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Papillary renal cell carcinoma (PRCC) is a significant kidney cancer with increasing incidence.
- The molecular mechanisms driving PRCC and effective therapeutic strategies remain incompletely understood.
- Identifying novel therapeutic targets and drugs is crucial for improving PRCC patient outcomes.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying PRCC development.
- To identify differentially expressed genes (DEGs) associated with PRCC.
- To predict potential anti-PRCC drugs using computational methods.
Main Methods:
- Differentially expressed genes (DEGs) were identified in PRCC.
- Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed for functional annotation.
- Connectivity Map (Cmap) was used to predict potential drugs based on DEGs.
- Drug-target, drug-pathway, and drug-protein interactions were integrated.
- Protein-protein interaction (PPI) analysis and molecular docking were conducted.
Main Results:
- 627 DEGs were identified in PRCC.
- KEGG analysis revealed significant associations with complement and coagulation cascades.
- 60 candidate drugs were predicted from the Cmap database.
- Vorinostat emerged as a promising drug candidate.
- Vorinostat demonstrated potential interactions with C3 and ANXN1, identified as upregulated hub genes and potential therapeutic targets.
Conclusions:
- The complement and coagulation cascades, along with cell adhesion molecules, significantly contribute to PRCC development and progression.
- Vorinostat shows considerable promise for PRCC treatment by targeting the C3 and ANXN1 proteins.
- Further investigation into vorinostat's efficacy in PRCC is warranted.
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