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Plant flavonoid 2' ,3,4' ,5,7-pentahydroxyflavone (morin hydrate), isolated from the family Moraceae (Morus alba L.), is known to have anti-inflammatory and anticancer effects. However, its pharmaceutical effects on metastasis have not been fully elucidated to date. Therefore, the current study investigated the effects of morin hydrate on cancer metastasis in MCF-7 human breast cancer cells. The results showed that morin hydrate suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-indu ced cell migration and invasion via the inhibition of matrix metalloproteinase (MMP)-9 activity. Furthermore, gene expression level of MMP-9, MMP-7, urokinase plasminogen activator (uPA), uPA receptor (uPAR) and fibronectin were significantly decreased by morin hydrate treatment. Morin hydrate inhibited the phosphorylation of Akt and glycogen synthase kinase (GSK)-3β, and downregulated the expression of an activator protein-1 subunit c-Fos. In addition, the GSK-3β phosphorylation and c-Fos expression were suppressed by PI3K/Akt pathway inhibitors, LY294002 and wortmannin. Taken together, these results demonstrated that morin hydrate reduced the metastatic potential in TPA-treated MCF-7 human breast cancer cells via the inhibition of MMPs, uPA and uPAR, and the underlying Akt/GSK-3β/c-Fos pathway. Therefore, the present investigation suggested that morin hydrate may be a natural substance with a preventive potential for metastasis in breast cancer cells.

Targeted therapy at the molecular level is important for pancreatic cancer treatment. This study looked over the anticancer activity of Orostachys japonicus in a human pancreatic cancer cell line, PANC‐1. An ethyl acetate fraction containing quercetin, kaempferol, and flavonol glycosides from O. japonicus (OJE) exhibited significant anticancer activity against the PANC‐1. OJE activated caspase‐3, caspase‐8, and caspase‐9, leading to the induction of both intrinsic and extrinsic apoptosis pathways. It also inhibited cyclin D1, cyclin B1, and cyclin‐dependent kinase 4, representing cell cycle arrest at both G1/S and G2/M phases. In addition, OJE phosphorylated MAPKs such as p38, JNK, and ERK, which are important upstream signaling factors in apoptosis and arrest of cell cycle inducing system. In conclusion, OJE effectively exerted antipancreatic cancer activity via induction of apoptosis directed by both intrinsic and extrinsic pathways and arrest of cell cycle regulated at both G1/S and G2/M stages, which is activated by MAPKs, p38, JNK, and ERK.

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