Retinoblastoma (Rb) is the most common pediatric malignant tumor of the eyes. Previous studies demonstrated that miR-491-3p is downregulated in various cancers. However, its function in Rb remains unknown. A total of 15 pairs of primary Rb tissues and adjacent noncancerous tissues were collected. Quantitative real-time PCR (qRT-PCR) was used to investigate the expression profiles of miR-491-3p. qRT-PCR, western blotting and in situ immunocytochemistry were performed to investigate the expression profiles of epithelial–mesenchymal transition-related proteins (E-cadherin, Vimentin and N-cadherin) in Rb tissues and Rb cell lines as well as cell morphology. Cell proliferation was estimated by MTS and colony formation assays. Apoptosis was determined by FACS, cell migration and invasion were analyzed using transwell chambers. MiR-491-3p’s target genes were predicted using target gene prediction databases. The interplay between miR-491-3p and SNN was evaluated through dual luciferase reporter gene assay. MiR-491-3p was significantly downregulated in mixed collection of 15 pairs of Rb tissues and Rb cell lines. Overexpression of miR-491-3p enhanced apoptosis, and significantly suppressed proliferation, migration and invasion of Rb cells. In contrast, the present of miR-491-3p inhibitor showed reversed results which apoptosis decreased, while cell proliferation of ARPE-19 cells increased. In addition, miR-491-3p increased the expression of E-cadherin, and dramatically decreased the expression of Vimentin and N-cadherin in Rb tissues and Rb cell lines, noticeable changes in morphology, too, as cells became less cohesive and more adhering. We found out that SNN was the pairing target of miR-491-3p and result showed that miR-491-3p and SNN interacted with each other. We also found out that the effects of miR-491-3p were in Rb cells were almost entirely canceled out at the overexpression of SNN. Our findings collectively suggest that miR-491-3p is an important tumor suppressor in Rb, which inhibits tumor growth and metastasis in Rb. These implicate it may be explored as a new therapeutic target in Rb.

视网膜母细胞瘤（Rb）是眼睛最常见的小儿恶性肿瘤。先前的研究表明，miR-491-3p在多种癌症中均被下调。但是，其在Rb中的功能仍然未知。总共收集了15对原发性Rb组织和相邻的非癌组织。实时定量PCR（qRT-PCR）用于研究miR-491-3p的表达谱。进行了qRT-PCR，western印迹和原位免疫细胞化学研究，以研究Rb组织和Rb细胞系中上皮-间质转化相关蛋白（E-cadherin，Vimentin和N-cadherin）的表达情况以及细胞形态。通过MTS和集落形成测定来估计细胞增殖。通过FACS确定细胞凋亡，使用transwell小室分析细胞迁移和侵袭。使用目标基因预测数据库预测了MiR-491-3p的目标基因。miR-491-3p和SNN之间的相互作用是通过双重荧光素酶报告基因分析评估的。在15对Rb组织和Rb细胞系的混合收集中，MiR-491-3p显着下调。miR-491-3p的过表达增强了细胞凋亡，并显着抑制了Rb细胞的增殖，迁移和侵袭。相反，miR-491-3p抑制剂的存在显示相反的结果，凋亡减少，而ARPE-19细胞的细胞增殖增加。此外，miR-491-3p可增加Rb组织和Rb细胞系中E-钙黏着蛋白的表达，并显着降低Vimentin和N-钙黏着蛋白的表达，并且随着细胞的凝聚力降低和粘附性增强，形态也发生明显变化。 。我们发现SNN是miR-491-3p的配对目标，结果表明miR-491-3p与SNN相互影响。我们还发现，在SNN的过表达中，miR-491-3p对Rb细胞的作用几乎被完全抵消了。我们的发现共同表明，miR-491-3p是Rb中重要的肿瘤抑制因子，可抑制Rb中的肿瘤生长和转移。这些暗示着它可以作为Rb中的新治疗靶标进行探索。