ABSTRACT
@#AIM: To explore the effect of silencing LncRNA DLGAP1-AS2 on the proliferation, migration and invasion of human retinoblastoma HXO-Rb44 and its possible mechanism.<p>METHODS: Twenty-five cases of retinoblastoma tissue specimens with complete clinical data and pathologically diagnosed were collected. At the same time, 9 cases of normal retinal tissue from which the eyeball was removed due to trauma were selected as controls. The qRT-PCR method was used to detect the expression of DLGAP1-AS2 and miR-1193 in normal retinal tissue, retinoblastoma tissue, human normal retinal vascular endothelial cell ACBRI-181, and retinoblastoma cell HXO-Rb44. The si-NC, si-DLGAP1-AS2, miR-NC, miR-1193 mimic, si-DLGAP1-AS2 and miR-1193 inhibitor(co-transfected)were transfected into HXO-Rb44 cells. The dual luciferase reporter experiment was used to detect the targeting relationship between DLGAP1-AS2 and miR-1193. The CCK-8 method, plate clone formation experiment and Transwell experiment were used to detect cell proliferation, colony formation, migration and invasion. Western blot method was used to detect the expression of E-cadherin and N-cadherin protein. <p>RESULTS: The expression of DLGAP1-AS2 in retinoblastoma tissue was higher than that of normal retinal tissue(<i>P</i><0.05), while the expression of miR-1193 was lower than that of normal retinal tissue(<i>P</i><0.05). The expression of DLGAP1-AS2 in HXO-Rb44 cells was higher than that of ACBRI-181 cells(<i>P</i><0.05), and the expression of miR-1193 was lower than that of ACBRI-181 cells(<i>P</i><0.05). DLGAP1-AS2 could target the expression of miR-1193. Transfection of si-DLGAP1-AS2 or miR-1193 mimic could inhibit the proliferation, migration and invasion of HXO-Rb44 cells. Co-transfection of si-DLGAP1-AS2 and miR-1193 inhibitor could reduce the effect of transfection of si-DLGAP1-AS2 on the proliferation, migration and invasion of HXO-Rb44 cells. <p>CONCLUSION: Silencing DLGAP1-AS2 could inhibit the proliferation, migration and invasion of retinoblastoma cells through targeted regulation of miR-1193 expression.