ABSTRACT
Objective@#To study the role of miR-18a in regulating the proliferation, migration and invasion of ovarian cancer cells through IGF-2/Akt pathway.@*Methods@#Ovarian cancer SKOV3 cells were cultured and grouped. The negative control group were not transfected with the plasmid, the blank plasmid group were transfected with the blank pcDNA3.1 plasmid, the IGF-2 plasmid group was transfected with the pcDNA3.1 plasmid expressing IGF-2, and the IGF-2 plasmid+L294002 group was transfected with pcDNA3.1 plasmid expressing IGF-2 and treated with Akt inhibitor LY294002. The upstream miRNA of IGF-2 was analyzed by bioinformatics method and verified by the double luciferase reporter gene method. The effect of overexpressing miR-18a on the expression of IGF-2 was observed.@*Results@#Transfection of IGF-2 expression plasmid can increase the expression level of IGF-2 in cells and the content of IGF-2 in culture medium (P<0.05) . Cell proliferation in the IGF-2 plasmid group (0.93±0.22, F=9.629, P<0.05) , migration (80.22±13.28, F=12.689, P<0.05) , invasion (72.31±11.38, F=33.845, P<0.05) , the relative expression levels of p-PI3K (1.35±0.22, F=8.321, P<0.05) and p-Akt (0.94±0.18, F=9.612, P<0.05) . The proliferation, migration, invasion viability, in the viability and cells were significantly higher than those in the negative control group and the blank plasmid group. And relative expression levels of p-PI3K and p-Akt in the IGF-2 plasmid+L294002 group were significantly lower than those in the IGF-2 plasmid group (P<0.05) . IGF-2 is a target gene of miR-18a, and overexpression of miR-18a can down-regulate the expression level of IGF-2 (P<0.05) .@*Conclusion@#IGF-2 can promote the proliferation, migration, and invasion of ovarian cancer cells, and this promotion is related to the activation of the Akt pathway, and miR-18a may be an upstream regulatory molecule of IGF-2.
ABSTRACT
Objective To study the role of miR-18a in regulating the proliferation, migration and inva-sion of ovarian cancer cells through IGF-2/Akt pathway. Methods Ovarian cancer SKOV3 cells were cultured and grouped. The negative control group were not transfected with the plasmid, the blank plasmid group were transfected with the blank pcDNA3.1 plasmid, the IGF-2 plasmid group was transfected with the pcDNA3.1 plas-mid expressing IGF-2, and the IGF-2 plasmid+L294002 group was transfected with pcDNA3.1 plasmid expressing IGF-2 and treated with Akt inhibitor LY294002. The upstream miRNA of IGF-2 was analyzed by bioinformatics method and verified by the double luciferase reporter gene method. The effect of overexpressing miR-18a on the expression of IGF-2 was observed. Results Transfection of IGF-2 expression plasmid can increase the expres-sion level of IGF-2 in cells and the content of IGF-2 in culture medium (P<0.05). Cell proliferation in the IGF-2 plasmid group(0.93±0.22, F=9.629, P<0.05), migration(80.22±13.28, F=12.689, P<0.05), invasion(72.31±11.38, F=33.845, P<0.05), the relative expression levels of p-PI3K(1.35±0.22, F=8.321, P<0.05) and p-Akt(0.94±0.18, F=9.612, P<0.05). The proliferation, migration, invasion viability, in the viability and cells were significantly higher than those in the negative control group and the blank plasmid group. And relative expression levels of p-PI3K and p-Akt in the IGF-2 plasmid+L294002 group were significantly lower than those in the IGF-2 plasmid group(P<0.05). IGF-2 is a target gene of miR-18a, and overexpression of miR-18a can down-regulate the expres-sion level of IGF-2(P<0.05). Conclusion IGF-2 can promote the proliferation, migration, and invasion of ovari-an cancer cells, and this promotion is related to the activation of the Akt pathway, and miR-18a may be an up-stream regulatory molecule of IGF-2.