IMRAN, M., ASLAM GONDAL, T., ATIF, M., SHAHBAZ, M., BATOOL QAISARANI, T., HANIF MUGHAL, M., SALEHI, B., MARTORELL, M., SHARIFI-RAD, J., SALEHI, B., CALINA, D., DOCEA, A. O., KOIRALA, N., ARYAL, S., LOMBARDO, D., PASQUA, L., TAHERI, Y., MARINA SALGADO CASTILLO, C., MARTORELL, M., MARTINS, N., IRITI, M., SULERIA, H. A. R., SHARIFI-RAD, J.:
Phytotherapy Research. 2020; 34: 1812– 1828.
Apigenin is an edible plant‐derived flavonoid that has been reported as an anticancer agent in several experimental and biological studies. It exhibits cell growth arrest and apoptosis in different types of tumors such as breast, lung, liver, skin, blood, colon, prostate, pancreatic, cervical, oral, and stomach, by modulating several signaling pathways. Apigenin induces apoptosis by the activation of extrinsic caspase‐dependent pathway by upregulating the mRNA expressions of caspase‐3, caspase‐8, and TNF‐α. It induces intrinsic apoptosis pathway as evidenced by the induction of cytochrome c, Bax, and caspase‐3, while caspase‐8, TNF‐α, and B‐cell lymphoma 2 levels remained unchanged in human prostate cancer PC‐3 cells. Apigenin treatment leads to significant downregulation of matrix metallopeptidases‐2, −9, Snail, and Slug, suppressing invasion. The expressions of NF‐κB p105/p50, PI3K, Akt, and the phosphorylation of p‐Akt decreases after treatment with apigenin. However, apigenin‐mediated treatment significantly reduces pluripotency marker Oct3/4 protein expression which might be associated with the downregulation of PI3K/Akt/NF‐κB signaling.