Clear cell renal cell carcinoma (ccRCC) is the most prevalent type of kidney cancer in adults, accompanied by an increasing incidence rate worldwide. We found that SBF2-AS1 was a differentially expressed long-noncoding RNA (lncRNA) in ccRCC through the microarray-based expression analyses. The aim of the present study was to explore the role of SBF2-AS1 in ccRCC development by assessing its effects on cellular processes and further investigate the underlying mechanism. SBF2-AS1 was found to be highly expressed in ccRCC tissues and cells. Ectopic expression and knockdown of SBF2-AS1 and miR-338-3p were performed in ccRCC 768-O cells to explore their effects on cell proliferation, migration, invasion, apoptosis and autophagy by EdU assay, scratch test, Transwell assay, calcein-AM/PI, and GFP-LC3 immunofluorescence assays, respectively. The interactions among SBF2-AS1, miR-338-3p and ETS1 were analyzed using dual-luciferase reporter, RIP and RNA pull-down assays. SBF2-AS1 specifically bound to miR-338-3p and inhibited its expression. Moreover, ETS1 was targeted by miR-338-3p. The knockdown of SBF2-AS1 or ETS1 or overexpression of miR-338-3p resulted in reduced cell proliferation, migration and invasion but elevated cell apoptosis and autophagy. In vivo experiments verified the tumor-suppressive role of silencing SBF2-AS1 in tumor growth of nude mice xenografted with ccRCC cells. Thus, silencing SBF2-AS1 exerted suppressive effects on ccRCC by elevating miR-338-3p and suppressing ETS1.

透明细胞肾细胞癌 (ccRCC) 是成人中最常见的肾癌类型，伴随着全球发病率的增加。我们通过基于微阵列的表达分析发现 SBF2-AS1 是 ccRCC 中差异表达的长链非编码 RNA (lncRNA)。本研究的目的是通过评估 SBF2-AS1 对细胞过程的影响并进一步研究其潜在机制来探索 SBF2-AS1 在 ccRCC 发展中的作用。发现 SBF2-AS1 在 ccRCC 组织和细胞中高表达。在ccRCC 768-O细胞中进行SBF2-AS1和miR-338-3p的异位表达和敲低，通过EdU试验、划痕试验、Transwell试验、钙黄绿素-AM探索它们对细胞增殖、迁移、侵袭、凋亡和自噬的影响/PI 和 GFP-LC3 免疫荧光测定，分别。使用双荧光素酶报告基因、RIP 和 RNA 下拉分析分析 SBF2-AS1、miR-338-3p 和 ETS1 之间的相互作用。SBF2-AS1 特异性结合 miR-338-3p 并抑制其表达。此外，ETS1 被 miR-338-3p 靶向。SBF2-AS1 或 ETS1 的敲低或 miR-338-3p 的过表达导致细胞增殖、迁移和侵袭减少，但细胞凋亡和自噬升高。体内实验证实了沉默 SBF2-AS1 在异种移植 ccRCC 细胞的裸鼠肿瘤生长中的肿瘤抑制作用。因此，沉默 SBF2-AS1 通过提高 miR-338-3p 和抑制 ETS1 对 ccRCC 发挥抑制作用。ETS1 被 miR-338-3p 靶向。SBF2-AS1 或 ETS1 的敲低或 miR-338-3p 的过表达导致细胞增殖、迁移和侵袭减少，但细胞凋亡和自噬升高。体内实验证实了沉默 SBF2-AS1 在异种移植 ccRCC 细胞的裸鼠肿瘤生长中的肿瘤抑制作用。因此，沉默 SBF2-AS1 通过提高 miR-338-3p 和抑制 ETS1 对 ccRCC 发挥抑制作用。ETS1 被 miR-338-3p 靶向。SBF2-AS1 或 ETS1 的敲低或 miR-338-3p 的过表达导致细胞增殖、迁移和侵袭减少，但细胞凋亡和自噬升高。体内实验证实了沉默 SBF2-AS1 在异种移植 ccRCC 细胞的裸鼠肿瘤生长中的肿瘤抑制作用。因此，沉默 SBF2-AS1 通过提高 miR-338-3p 和抑制 ETS1 对 ccRCC 发挥抑制作用。