A Network Pharmacology Study to Uncover the Mechanism of FDY003 for Ovarian Cancer Treatment

Abstract

Ovarian cancer (OC) is one of the deadliest gynecological tumors responsible for 0.21 million deaths per year worldwide. Despite the increasing interest in the use of herbal drugs for cancer treatment, their pharmacological effects in OC treatment are not understood from a systems perspective. Using network pharmacology, we determined the anti-OC potential of FDY003 from a comprehensive systems view. We observed that FDY003 suppressed the viability of human OC cells and further chemosensitized them to cytotoxic chemotherapy. Through network pharmacological and pharmacokinetic approaches, we identified 16 active ingredients in FDY003 and their 108 targets associated with OC mechanisms. Functional enrichment investigation revealed that the targets may coordinate diverse cellular behaviors of OC cells, including their growth, proliferation, survival, death, and cell cycle regulation. Furthermore, the FDY003 targets are important constituents of diverse signaling pathways implicated in OC mechanisms (eg, phosphoinositide 3-kinase [PI3K]-Akt, mitogen-activated protein kinase [MAPK], focal adhesion, hypoxia-inducible factor [HIF]-1, estrogen, tumor necrosis factor [TNF], erythroblastic leukemia viral oncogene homolog [ErbB], Janus kinase [JAK]-signal transducer and activator of transcription [STAT], and p53 signaling). In summary, our data present a comprehensive understanding of the anti-OC effects and mechanisms of action of FDY003.