PRC1 gene silencing inhibits proliferation, invasion, and angiogenesis of retinoblastoma cells through the inhibition of the Wnt/β‐catenin signaling pathway

: Retinoblastoma is an ocular malignancy occurring in childhood. The current study evaluates the ability of silenced PRC1 on retinoblastoma cell proliferation, and angiogenesis via the Wnt/β-catenin signaling pathway. A total of 36 cases of retinoblastoma tissues (n = 36) and normal retinal tissues (n = 10) were selected in the current study. Retinoblastoma cells presenting with the high PRC1 messenger RNA (mRNA) expression were selected among the WERI-Rb-1, HXO-RB44, Y79, SO-Rb50, and SO-Rb70 cells lines, and were transfected with siRNA-PRC1 and LiCl (the activator of the Wnt/β-catenin pathway). The expressions of PRC1, VEGF, Wnt1, β-catenin, CyclinD1, extent of β-catenin, and GSK-3β phosphorylation were evaluated. Cell proliferation, cell-cycle distribution, and cell invasion of retinoblastoma cells were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and Transwell assay. The angiogenesis of retinoblastoma cells was detected by tube formation assay. HXO-RB44 and WERI-Rb-1 cells were selected owing to the highest PRC1 mRNA expression. Meanwhile, PRC2 gene silencing presented lower expression levels of PRC1, VEGF, Wnt1, β-catenin, CyclinD1, extent of β-catenin and GSK-3β phosphorylation, decreased proliferation and invasion abilities, extended G0/G1 phase, and shortened S and G2/M phases of HXO-RB44 and WERI-Rb-1 cells, suggesting the silenced PRC2 inactivated Wnt/β-catenin pathway, so as to further restrain the retinoblastoma cell proliferation, invasion, and angiogenesis. These results support the view that PRC1 gene silencing could suppress the proliferation, and angiogenesis of retinoblastoma cells by repressing the Wnt/β-catenin pathway.