Abstract:

Objective To investigate the role of long non-coding RNA family with sequence similarity 83 member A antisense RNA 1 in retinoblastoma （RB） cells and its potential molecular mechanism. Methods RB cells were cultured in vitro， and Vector， pcDNA-FAM83A-AS1， NC-siRNA， and FAM83A-AS1-siRNA were transfected into cells to detect the expression of FAM83A-AS1， RB cell proliferation ability， and apoptosis rate in RB cells. Bioinformatics and dual-luciferase reporter gene experiments were performed to predict and verify the targeting relationship between FAM83A-AS1 and miR-150， and miR-150 and the high-mobility family protein A2 （HMGA 2）. The expression of miR-150 and HMGA2 mRNA in RB cells was measured by RT-qPCR； HMGA 2 protein in RB cells by Western blot； and the proliferation and apoptotic capacity of RB cells after transfection by MTT assay and flow cytometry. Results The expression of FAM83A-AS1 in the pcDNA-FAM83A-AS1 group was significantly higher than that of the Vector group and lower than that of the NC-siRNA group （P < 0.05）. The cell proliferation capacity in the pcDNA-FAM83A-AS1 group was significantly higher， and the apoptosis rate was significantly lower （P < 0.05）. Compared with NC-siRNA group， FAM83A-AS1-siRNA group showed significantly increased apoptosis rate （P < 0.05）. The miR-150 mimic significantly inhibited the proliferation capacity of RB cells and promoted cell apoptosis. However， pcDNA-HMGA 2 significantly reversed the effect of miR-150 mimic on the proliferation and apoptosis of RB cells. Conclusion Knockdown of lncRNA FAM83A-AS1 inhibited RB cell proliferation and promoted apoptosis by regulating the miR-150/HMGA2 axis.

Key words: lncRNA FAM83A-AS1, retinoblastoma, miR-150, proliferation, apoptosis