Multiple molecular and cellular mechanisms of the antitumour effect of dihydromyricetin (Review)

Abstract

Dihydromyricetin (DHM) is a natural flavonoid compound with multiple antitumour effects, including inhibition of proliferation, promotion of apoptosis, inhibition of invasion and migration, clearance of reactive oxygen species (ROS) and induction of autophagy. For example, DHM can effectively block the progression of the tumour cell cycle and inhibit cell proliferation. In different types of cancer cells, DHM can regulate the PI3K/Akt pathway, mTOR, and NF-κB pathway components, such as p53, and endoplasmic reticulum stress can alter the accumulation of ROS or induce autophagy to promote the apoptosis of tumour cells. In addition, when DHM is used in combination with various known chemotherapy drugs, such as paclitaxel, nedaplatin, doxorubicin, oxaliplatin and vinblastine, it can increase the sensitivity of tumour cells to DHM and increase the therapeutic effect of chemotherapy drugs. In the present review, the multiple molecular and cellular mechanisms underlying the antitumour effect of DHM, as well as its ability to increase the effects of various traditional antitumour drugs were summarized. Through the present review, it is expected by the authors to draw attention to the potential of DHM as an antitumour drug and provide valuable references for the clinical translation of DHM research and the development of related treatment strategies.