Nutraceutical Iridoid Glycoside Monotropein Induces Apoptosis and Suppresses PI3K/Akt/mTOR Signaling in Breast Cancer Cells: An In Vitro Evaluation
Jin Che, Xiaoxu Han, Xiaomin LiBackground
The rising global burden of breast cancer, marked by increasing incidence and mortality rates, has intensified the pursuit of anti-cancer agents that are both effective and mechanistically targeted while minimizing systemic toxicity. In this context, nutraceuticals are being explored for their therapeutic potential due to their capacity to influence multiple oncogenic and survival pathways, their favorable safety profiles, and their potential to complement or enhance conventional chemotherapeutic approaches. Monotropein, a plant-derived iridoid glycoside, has garnered considerable interest owing to its diverse pharmacological activities, including anti-inflammatory, antioxidant, and cytoprotective effects. Despite these documented bioactivities, the specific anti-cancer mechanisms of monotropein, particularly in the context of breast carcinoma, remain inadequately explored.
Purpose
The present study aims to elucidate the anti-cancer potential of monotropein in a breast adenocarcinoma cell line.
Materials and Methods
The anti-cancer potential of monotropein was assessed using an
Results
Our findings demonstrated that monotropein exhibited selective anti-cancer activity against breast cancer cells. Increased caspase activity and elevated Bax levels, accompanied by a decline in the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), were observed in the MCF-7 cells treated with monotropein. Furthermore, monotropein treatment significantly downregulated PI3K, Akt, and mTOR protein expression. Collectively, these findings demonstrate that monotropein exerted an anti-cancer effect in the breast adenocarcinoma cell line through the activation of the apoptotic cascade and suppression of PI3K/Akt/mTOR signaling.
Conclusion
These findings highlight monotropein’s potential as a nutraceutical-based therapeutic candidate, although further investigations are required to validate its efficacy and underlying mechanisms in advanced pre-clinical models.