Identification of Potential Molecular Targets of Doxorubicin for Application in Skin Cancer: A Network Pharmacology and Molecular Docking Perspective
The primary objective was to find the pharmacological targets of doxorubicin and their mechanisms of action, with a dual focus on their therapeutic relevance in skin cancer treatment and their potential involvement in resistance to doxorubicin in cancer cells. The targets of skin cancer and potential targets of doxorubicin were searched from multiple databases. Common targets were chosen using the GeneVenn tool and then imported into the STRING database to construct a protein-protein interaction network. Topological factors were evaluated with Cytoscape to identify core targets. FunRich was used to identify the signaling pathways, molecular functions, cellular components, and biological processes involving the top targets. Molecular docking was conducted using the Molecular Operating Environment software. The top five target genes identified as therapeutic targets of doxorubicin for treatment of skin cancer are poly(ADP-ribose) polymerase, epidermal growth factor receptors, heat shock protein 90 alpha family class A member 1, Harvey rat sarcoma viral oncogene homolog, and mammalian target of rapamycin. In addition, doxorubicin-induced resistance mechanisms were also predicted. Further research on innovative methods of delivering doxorubicin to maximize its effectiveness in treating skin cancer and to prevent the development of resistance to the drug is necessary.
Authors
- Mohd Ashif Khan (ORCID: https://orcid.org/0000-0003-1576-8779)
- Sonali Karhana (ORCID: https://orcid.org/0009-0000-8532-3180)
- Javed Ali (ORCID: https://orcid.org/0000-0001-5308-0655)
- Sanjula Baboota (ORCID: https://orcid.org/0000-0003-1508-6786)
Institutions
- Jamia Hamdard (IN)
Publication Details
- Journal
- Assay and Drug Development Technologies
- Published
- 2025-06-30
- DOI
- https://doi.org/10.1089/adt.2024.083
- Primary Topic
- Synthesis and biological activity
- Type
- article
- Field-Weighted Citation Impact
- 0.00