Mechanism of FGF7 gene silencing in regulating viability, apoptosis, invasion of retinoblastoma cell line HXO-Rb44 and angiogenesis.

Abstract

To explore the mechanism of fibroblast growth factor 7 (FGF7) gene silencing in regulating viability, apoptosis, invasion of retinoblastoma (RB) cell line HXO-Rb44 and angiogenesis. Human normal retinal vascular endothelial cells ACBRI-181 was set as the normal group. The cultured RB cell lines HXO-Rb44 were divided into three groups: the blank group (without plasmid transfection), negative control group (transfection of FGF7 plasmid), and the si-FGF7 group (transfection of FGF7 siRNA plasmid). Quantitative Real Time-Polymerase Chain Reaction and Western blot were used to measure the mRNA and protein expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), angiopoietin-2 (Ang-2), and proliferating cell nuclear antigen (PCNA) in each group. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell invasion assay, and flow cytometry were used, respectively, to assess cell viability, invasive capability, and cell apoptosis in each group. The mRNA and protein expression of FGF7, Bcl-2, VEGF, bFGF, Ang-2, and PCNA were significantly decreased, and the mRNA and protein expression of Bax were significantly increased in the si-FGF7 group than in the blank group (all p<0.05). Compared with the blank group, the si-FGF7 group had significantly decreased cells invasive capability, cell viability at 48 h and 72 h and proliferation, and significantly increased apoptosis rate (all p<0.05). FGF7 gene silencing can inhibit the viability and invasion of RB cells and the expression of angiogenesis-related factors and can promote RB apoptosis.