Myricetin-induced apoptosis in triple-negative breast cancer cells through inhibition of the PI3K/Akt/mTOR pathway

Breast cancer is still a severe origin of malignant demise in females, and its prevalence is rising worldwide. Triple-negative breast cancer (TNBC) is a diversified aggressive breast tumor distinguished by inadequate prognosis, early recurrence, high invasion, and extremely metastasized disease. Chemotherapy is being used to treat it; however, it has low efficacy. On the other hand, with the growing number of corroborations on subtypes of TNBC and molecular biology of tumors, significant advancement in TNBC targeted treatment has been made. Myricetin (MYR), a polyhydroxyflavonol compound widely found in nature, has been shown to possess anticancer effects in various cancers. Though, the mechanisms and impacts of MYR on metastasis of TNBC remain unclear. Early and late apoptotic cell death and cell proliferation inhibition were observed in MYR-treated TNBC cells. MYR modulated cell cycle, pro-angiogenic, and invasion effects via the mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Protein kinase B (PKB/also known as AKT) signaling pathways. Moreover, it regulates the expression of MAPK, PI3K/AKT/mTOR, I kappa B/NF-kappa B, Hippo, STAT3, GSK-3 beta, Nrf2/HO-1, TLR, eNOS / NO, ACE, and AChE. Here, we review the anticancer effects of MYR for TNBC and target the PI3K/AKT/mTOR pathway as a therapeutic target for the fruitful treatment of TNBC to summarize MYR's therapeutic potential.

Automated summary

Breast cancer is a major cause of malignant death in females, and triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis. Myricetin (MYR), a naturally occurring compound, has been found to have anti-cancer effects in various cancers, including TNBC. It regulates multiple signaling pathways to inhibit cell proliferation and invasion and promote cell apoptosis. The PI3K/AKT/mTOR pathway is identified as a potential therapeutic target for MYR in TNBC treatment.