Piceatannol Inhibits Viability and Enhances Apoptosis in Kidney Cancer A498 Cells via Activating Caspases and Downregulating PI3K/AKT/mTOR Pathway

Background Kidney cancer constitutes a considerable worldwide health issue, significantly contributing to cancer-associated morbidity and mortality. Despite numerous advancements, existing treatment modalities for kidney cancer pose significant hurdles, including limited efficacy and elevated recurrence rates, necessitating safer and more effective alternative therapies. Purpose The current work was dedicated to studying the anti-cancer properties of piceatannol against kidney cancer cells. Materials and Methods The cytotoxic efficacy of piceatannol at varying dosages (5–100 µM) on renal cancer A498 cell viability was assessed utilizing the MTT test. The level of apoptotic incidence in control and piceatannol-treated A498 cells was assessed using a dual staining method. The caspase enzymes and the phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mammalian target of rapamycin (mTOR) protein levels in the untreated and piceatannol-treated A498 cells were evaluated using commercial kits. Results The results of the MTT assay suggested that piceatannol administration dose-dependently reduced A498 cell viability. The piceatannol administration increased the incidence of apoptosis in A498 cells, as evidenced by the dual-staining assay results. Furthermore, the piceatannol treatment enhanced the caspase-3, -8, and -9 levels and diminished the PI3K, AKT, and mTOR levels in the A498 cells. Conclusion The findings of this study suggested the anti-cancer effects of piceatannol against renal cell carcinoma. The development of piceatannol as a potential therapeutic option requires further validation. This study provides a foundation to understand the molecular mechanisms by which piceatannol affects A498 cells, warranting more studies into its role in renal cancer management.