Previous studies have proven that long intergenic non-coding RNA regulator of reprogramming (Linc-ROR) plays opposing roles in different cancer types. This work intended to investigate its functions and underlying mechanisms in gastric carcinoma (GCa) progression. RT-qPCR was utilized for gene expression measurement. GCa cell viability, apoptosis, migration, and invasion were detected by functional assays, including CCK-8, flow cytometry, and Transwell assays. ChIP assay and Dual-luciferase reporter assay were utilized to affirm the associations between genes. Linc-ROR expression dramatically declined in GCa tissues and cell lines. Linc-ROR upregulation suppressed GCa cell proliferation, migration, and invasion but accelerated GCa cell apoptosis. As for Linc-ROR-associated molecular mechanisms in GCa, SOX2 associated with Linc-ROR promoter region to activate Linc-ROR transcription in GCa cells; Linc-ROR upregulated ANXA10 level in GCa cells by competitively binding to miR-580-3p. As revealed by rescue assays, Linc-ROR-induced inhibition on malignant biological behaviors of GCa cells could be partially abated by ANXA10 deletion or miR-580-3p upregulation. SOX2-activated Linc-ROR serves as a cancer suppressor to restrain GCa progression in vitro via the miR-580-3p/ANXA10 pathway, suggesting a promising diagnostic and therapeutic target for GCa patients.

先前的研究已经证明，长链基因间非编码 RNA 重编程调节因子 (Linc-ROR) 在不同的癌症类型中起着相反的作用。这项工作旨在研究其在胃癌 (GCa) 进展中的功能和潜在机制。RT-qPCR 用于基因表达测量。GCa 细胞活力、细胞凋亡、迁移和侵袭通过功能测定检测，包括 CCK-8、流式细胞术和 Transwell 测定。ChIP 测定和双荧光素酶报告测定用于确认基因之间的关联。Linc-ROR 表达在 GCa 组织和细胞系中显着下降。Linc-ROR 上调抑制 GCa 细胞增殖、迁移和侵袭，但加速 GCa 细胞凋亡。至于 GCa 中 Linc-ROR 相关的分子机制，SOX2 与 Linc-ROR 启动子区域相关，可激活 GCa 细胞中的 Linc-ROR 转录；Linc-ROR 通过竞争性结合 miR-580-3p 上调 GCa 细胞中的 ANXA10 水平。正如救援试验所揭示的那样，Linc-ROR 诱导的对 GCa 细胞恶性生物学行为的抑制可以通过 ANXA10 缺失或 miR-580-3p 上调来部分减轻。SOX2 激活的 Linc-ROR 作为癌症抑制剂通过 miR-580-3p/ANXA10 途径在体外抑制 GCa 进展，表明 GCa 患者有希望的诊断和治疗靶点。ANXA10 缺失或 miR-580-3p 上调可部分减轻 Linc-ROR 诱导的对 GCa 细胞恶性生物学行为的抑制。SOX2 激活的 Linc-ROR 作为癌症抑制剂通过 miR-580-3p/ANXA10 途径在体外抑制 GCa 进展，表明 GCa 患者有希望的诊断和治疗靶点。ANXA10 缺失或 miR-580-3p 上调可部分减轻 Linc-ROR 诱导的对 GCa 细胞恶性生物学行为的抑制。SOX2 激活的 Linc-ROR 作为癌症抑制剂通过 miR-580-3p/ANXA10 途径在体外抑制 GCa 进展，表明 GCa 患者有希望的诊断和治疗靶点。