Renal cell carcinoma (RCC), one of the most common types of kidney cancer, represents a major global health concern due to its increasing incidence and high death rates. While conventional treatment modalities have improved patient outcomes, they often face limitations such as drug resistance, severe adverse effects, and limited efficacy in advanced or metastatic cases. These challenges highlight the urgent need for novel therapeutic approaches to enhance RCC management. Tricetin, a natural flavonoid abundant in cereal plants, has shown promising anticancer activity in various malignancies by inhibiting cancer cell proliferation, migration, and invasion. However, the molecular mechanisms underlying Tricetin's effects on RCC remain poorly understood. In this research, we employed network pharmacology to identify key molecular targets of Tricetin in RCC and evaluated its binding affinity to these targets using molecular docking techniques. Bioinformatics analyses were conducted to predict the potential biological pathways involved. Furthermore, in vitro experiments using RCC cell lines (786-O and ACHN) demonstrated that Tricetin suppresses cell proliferation and migration, likely through modulation of the EGFR/PI3K/Akt signaling pathway. Overall, our findings offer new insights into the therapeutic potential of Tricetin and provide a foundation for developing targeted treatment strategies to improve RCC outcomes.