Eriodictyol, a naturally occurring flavanone, has appeared as a biologically versatile compound with increasing relevance in biomedical research, especially in cancers. Evidence over the past few decades indicates that eriodictyol influences cancer cell fate through coordinated modulation of cell-cycle control, survival, and regulated cell death pathways. Eriodictyol appears to reshape oncogenic signaling networks, including PI3K/Akt/mTOR and associated kinase cascades, thereby restricting proliferative capacity and lowering resistance thresholds. Studies consistently report cell-cycle arrest at critical checkpoints, accompanied by activation of both mitochondrial- and death-receptor-mediated apoptotic pathways through disruption of BCL-2 family balance, caspase engagement, and mitochondrial destabilization. Furthermore, eriodictyol alters intracellular redox dynamics in a dose-dependent manner, selectively sensitizing cancer cells to oxidative and metabolic stress. More recent findings extend its significance to inflammation-driven tumor progression and to the regulation of ferroptosis. Beyond intrinsic pharmacological activity, advances in nanocarrier-based delivery and balanced combination strategies have started to address critical challenges and limitations regarding solubility and bioavailability, while allowing precise therapeutic applications. In this review, we have discussed the plausible mechanisms, experimental evidence, and translational insights of eriodictyol as a systems-level modulator of cancer biology. We also outlined research priorities essential for progressing its clinical relevance as future perspectives.
Mumtaz et al. (Tue,) studied this question.