Apigenin inhibits proliferation, migration, invasion and epithelial mesenchymal transition of glioma cells by regulating miR-103a-3p/NEED9/AKT axis

• Autor(a) principal: WAN,Jing
• Data de Publicação: 2022
• Outros Autores: HUANG,Min
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000101128
• topic: apigenin; proliferation; migration; invasion; epithelial mesenchymal transition; glioma

Abstract Apigenin is one kinds of natural flavonoids from plants. Many researches showed this compound has potential antioxidant, anti-inflammatory and anticancer functions. This study aimed to investigate the effects of apigenin on proliferation, migration, invasion, epithelial mesenchymal transition (EMT) in glioma cells, and to reveal the underlying mechanism of apigenin. MTT assay indicated the proliferation rate of glioma cells U251 was significantly decreased with the treatment of apigenin in a dose-dependent manner. In addition, apigenin could inhibit the cell invasion, wound healing and decrease the expression of EMT-related proteins, NEDD9, p-FAK and p-AKT. Quantitative real-time PCR showed miR-103a-3p was remarkably increased in the presence of apigenin. Inhibition of miR-103a-3p attenuated the effects of apigenin on U251 cells. Dual-luciferase assay and western blot further demonstrated that NEDD9 was a direct target of miR-103a-3p. Moreover, knockdown NEDD9 almost reversed the activities of silenced miR-103a-3p in transwell invasion, wound healing and regulation of NEDD9/FAK/AKT axis. In conclusion, apigenin could inhibit glioma cell proliferation, migration, invasion and EMT via activating of miR-103a-3p and targeting NEDD9/FAK/AKT pathway.