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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. [ABSTRACT FROM AUTHOR]