Published online Dec 20, 2023. doi: 10.5493/wjem.v13.i5.142
Peer-review started: September 22, 2023
First decision: September 29, 2023
Revised: October 4, 2023
Accepted: October 30, 2023
Article in press: October 30, 2023
Published online: December 20, 2023
Bitter melon has been used to stop the growth of breast cancer (BRCA) cells. However, the underlying mechanism is still unclear.
The motivation of this research is to explore the underlying pharmacological mechanisms.
The goal of this study was to predict the therapeutic effect of bitter melon against BRCA using network pharmacology.
The active ingredients of bitter melon and the related protein targets were taken from the Indian Medicinal Plants, Phytochemistry and Therapeutics and SuperPred databases, respectively. The GeneCards database has been searched for BRCA-related targets. Through an intersection of the drug’s targets and the disease’s objectives, prospective bitter melon anti-BRCA targets were discovered. Gene ontology and kyoto encyclopedia of genes and genomes enrichment analyses were carried out to comprehend the biological roles of the target proteins. The binding relationship between bitter melon’s active ingredients and the suggested target proteins was verified using molecular docking techniques.
Through the active ingredient-anti-BRCA target network analysis, three major components were found to be important in mediating the putative anti-BRCA actions of bitter melon: momordicoside K, kaempferol, and quercetin. In the protein-protein interaction network analysis, the top three proteins were determined to be heat shock protein 90 AA, proto-oncogene tyrosine-protein kinase, and signal transducer and activator of transcription 3 (STAT3). According to molecular docking research, the principal active phytochemicals in bitter melon are able to bind to HAP90AA1, STAT3, and other breast cancer-related targets.
Overall, the integration of network pharmacology, molecular docking, and functional enrichment analyses shed light on potential mechanisms underlying bitter melon’s ability to fight BRCA, implicating active ingredients and protein targets, as well as highlighting the major signaling pathways that may be altered by this natural product for therapeutic benefit.
Database resources were used to examine active compounds found in bitter melon. Network pharmacology and molecular docking techniques were used to explore the mechanism through which bitter melon was used to treat BRCA. Momordicoside K, kaempferol, and quercetin were identified as potentially important active ingredients of bitter melon showing anti-BRCA actions. The study identified several possible molecular targets as well as signaling pathways involved in bitter melon’s anti-BRCA actions, like phosphatidylinositol 3-kinase/protein kinase B signaling and janus kinase-signal transducer and activator of transcription signaling. The study suggests further experimental verification to confirm the potential findings of bitter melon in the treatment of BRCA.