Retinoblastoma is the most common malignancy in children's eyes with high incidence. Long non-coding RNAs (lncRNAs) play important roles in the progression of retinoblastoma. LncRNA FEZF1 antisense RNA 1 (FEZF1-AS1) has been found to stimulate retinoblastoma. However, the mechanism of FEZF1-AS1 underlying progression of retinoblastoma is still unclear. In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells. FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. In conclusion, FEZF1-AS1 elevated growth and inhibited apoptosis by regulating miR-363-3p/PAX6 in retinoblastoma, which provide a new target for retinoblastoma treatment.

视网膜母细胞瘤是儿童眼中最常见的恶性肿瘤，发病率很高。长链非编码 RNA (lncRNA) 在视网膜母细胞瘤的进展中起重要作用。已发现 LncRNA FEZF1 反义 RNA 1 (FEZF1-AS1) 可刺激视网膜母细胞瘤。然而，FEZF1-AS1 在视网膜母细胞瘤进展中的潜在机制仍不清楚。在目前的研究中，FEZF1-AS1 在视网膜母细胞瘤组织和细胞中上调。FEZF1-AS1过表达增强视网膜母细胞瘤细胞活力，促进细胞周期，抑制细胞凋亡。相反，FEZF1-AS1 敲低降低了细胞活力、周期和细胞凋亡增加。证实了 FEZF1-AS1 和 microRNA-363-3p (miR-363-3p) 之间的相互作用。FEZF1-AS1 下调 miR-363-3p 并上调 PAX6。PAX6 是 miR-363-3p 的靶基因。EZF1-AS1 通过 PAX6 促进视网膜母细胞瘤细胞活力并抑制细胞凋亡。此外，我们证明 FEZF1-AS1 有助于体内肿瘤形成。总之，FEZF1-AS1通过调节视网膜母细胞瘤中的miR-363-3p/PAX6来促进生长并抑制细胞凋亡，这为视网膜母细胞瘤的治疗提供了新的靶点。