circRNAs have been considered as a rising factor in cancers. However, the roles and mechanisms of circ-sirt1 in gastric cancer (GC) remain largely unknown. In this study, we found that the expressions of sirt1 and circ-sirt1 are decreased in tissues or serums of GC patients by real-time quantitative PCR (RT-qPCR). The expressions of miR-132-3p/miR-212-3p showed an opposite tendency in these samples. The co-transfection of miR-132-3p/miR-212-3p mimics counteracted the enhancement of sirt1 expression induced by circ-sirt1. The results of cell colony-formation assay and Transwell assays demonstrated that the proliferation, migration, and invasion activities of BGC-823 cells were inhibited by circ-sirt1 overexpression or miR-132-3p/miR-212-3p knockdown, respectively. The xenograft tumor model result indicated that the circ-sirt1 overexpression suppressed the tumor growth of BGC-823 cells. The regulation of miR-132-3p/miR-212-3p between circ-sirt1 and sirt1 was verified in the mice tumor tissues. Thus, circ-sirt1 inhibited tumor growth and invasion probably by sponging miR-132-3p/miR-212-3p and upregulating sirt1 expression in GC. These findings may provide a theoretical basis for the classification of GC and a novel therapeutic target for GC patients.

中文翻译：

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Circ-sirt1 通过海绵化 miR-132-3p/miR-212-3p 和上调 sirt1 表达来抑制胃癌的生长和侵袭。

circRNAs被认为是癌症的一个上升因素。然而，circ-sirt1 在胃癌 (GC) 中的作用和机制仍然很大程度上未知。在本研究中，我们通过实时定量 PCR (RT-qPCR) 发现 GC 患者的组织或血清中 sirt1 和 circ-sirt1 的表达降低。miR-132-3p/miR-212-3p的表达在这些样品中表现出相反的趋势。miR-132-3p/miR-212-3p 模拟物的共转染抵消了 circ-sirt1 诱导的 sirt1 表达增强。细胞集落形成试验和 Transwell 试验的结果表明，BGC-823 细胞的增殖、迁移和侵袭活性分别受到 circ-sirt1 过表达或 miR-132-3p/miR-212-3p 敲低的抑制。异种移植肿瘤模型结果表明circ-sirt1过表达抑制了BGC-823细胞的肿瘤生长。在小鼠肿瘤组织中验证了 circ-sirt1 和 sirt1 之间 miR-132-3p/miR-212-3p 的调节。因此，circ-sirt1 可能通过海绵化 miR-132-3p/miR-212-3p 和上调 GC 中的 sirt1 表达来抑制肿瘤生长和侵袭。这些发现可能为GC的分类提供理论基础，并为GC患者提供新的治疗靶点。