• Int J Med Sci · Jan 2024

    Arbutin overcomes tumor immune tolerance by inhibiting tumor programmed cell death-ligand 1 expression.

    • Ching-Han Liu, Jing-Ru Weng, Li-Hsien Wu, Rui-Yang Song, Ming-Der Huang, Xin-He Wu, Chia C Wang, and Che-Hsin Lee.
    • Division of Cardiology, Department of Internal Medicine, Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan.
    • Int J Med Sci. 2024 Jan 1; 21 (15): 299230022992-3002.

    AbstractArbutin, predominantly derived from the bearberry plant, exhibits promising immunomodulatory properties. Given its ability to influence the programmed cell death-ligand 1/ programmed cell death-1 (PD-L1/PD-1) pathway, it is emerging as a potential alternative treatment for cancer. A reduced expression of PD-L1, as seen after arbutin treatment, can bolster immune responses critical step in effective tumor immunotherapy. However, the molecular mechanism by which arbutin inhibits PD-L1 is still incompletely known. The expression of PD-L1 was decreased after tumor cells were treated with arbutin. Arbutin can downregulate the expression of PD-L1 on the cell surface via the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. The findings suggest the protective role of arbutin and provide novel insights into immunotherapy, which involves inhibiting the AKT/mTOR signaling pathway. Arbutin might serve as a potential therapeutic agent alone or in combination with other treatments.© The author(s).

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