Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chinese Traditional and Herbal Drugs ; (24): 2371-2376, 2019.
Artigo em Chinês | WPRIM | ID: wpr-851126

RESUMO

Objective: To investigate the effects of the combination of Celastrus orbiculatus extracts and miR-302 on proliferation, invasion and migration of human esophageal cancer cells and the regulation of PI3K/Akt signaling pathway. Methods Quantitative RT-PCR was used to detect the expression of miR-302 in human normal esophageal epithelial cells Het-1A and different esophageal cancer cell lines. The miR-302 mimic and negative control mimic control were transfected into human esophageal cancer TE-1 cells, and qPCR was used to detect the expression of miR-302 in TE-1 cells after plasmid transfection. TE-1 cells were treated with C. orbiculatus extracts alone and combination treatment. The proliferation of TE-1 cells was detected by CCK-8 assay. The invasion and migration of TE-1 cells were detected by Transwell assay. Western blot analysis of the expression of related protein in the PI3K/Akt signaling pathway was carried out. Results: The expression of miR-302 in esophageal cancer cell lines was significantly lower than that in esophageal epithelial cells (P < 0.05). Transfection of miR-302 mimic could effectively increase the expression of miR-302 in TE-1 cells (P < 0.05). The use of C. orbiculatus extracts alone or overexpression of miR-302 inhibited proliferation, invasion and migration of esophageal cancer TE-1 cells (P < 0.05), down-regulated PI3K and p-Akt protein expression; Combination treatment had more significant effect on inhibiting proliferation, invasion and migration of TE-1 cells and down-regulating protein expression of PI3K and p-Akt (P < 0.05). Conclusion: Celastrus orbiculatus extracts combined with miR-302 can synergistically inhibit the proliferation, invasion, and migration of esophageal cancer TE-1 cells, and its mechanism may be related to the inhibition of PI3K/Akt signaling pathway activation.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA