Myasthenia gravis (MG) is an autoimmune disorder resulting from antibodies against the proteins at the neuromuscular junction. Emerging evidence indicates that long non-coding RNAs (lncRNAs), acting as competing endogenous RNAs (ceRNAs), are involved in various diseases. However, the regulatory mechanisms of ceRNAs underlying MG remain largely unknown. In this study, we constructed a lncRNA-mediated ceRNA network involved in MG using a multi-step computational strategy. Functional annotation analysis suggests that these lncRNAs may play crucial roles in the immunological mechanism underlying MG. Importantly, through manual literature mining, we found that lncRNA SNHG16 (small nucleolar RNA host gene 16), acting as a ceRNA, plays important roles in the immune processes. Further experiments showed that SNHG16 expression was upregulated in peripheral blood mononuclear cells (PBMCs) from MG patients compared to healthy controls. Luciferase reporter assays confirmed that SNHG16 is a target of the microRNA (miRNA) let-7c-5p. Subsequent experiments indicated that SNHG16 regulates the expression of the key MG gene interleukin (IL)-10 by sponging let-7c-5p in a ceRNA manner. Furthermore, functional assays showed that SNHG16 inhibits Jurkat cell apoptosis and promotes cell proliferation by sponging let-7c-5p. Our study will contribute to a deeper understanding of the regulatory mechanism of MG and will potentially provide new therapeutic targets for MG patients.

重症肌无力（MG）是一种自身免疫性疾病，由针对神经肌肉接头处蛋白质的抗体引起。新兴证据表明，充当竞争性内源性RNA（ceRNA）的长非编码RNA（lncRNA）与多种疾病有关。但是，MG的ceRNA的调控机制仍然未知。在这项研究中，我们使用多步计算策略构建了一个参与MG的lncRNA介导的ceRNA网络。功能注释分析表明，这些lncRNA可能在MG的免疫机制中起关键作用。重要的是，通过手工文献挖掘，我们发现作为ceRNA的lncRNA SNHG16（小核仁RNA宿主基因16）在免疫过程中起着重要作用。进一步的实验表明，与健康对照组相比，MG患者外周血单核细胞（PBMC）中的SNHG16表达上调。萤光素酶报告基因测定证实SNHG16是microRNA（miRNA）let-7c-5p的靶标。随后的实验表明，SNHG16通过以ceRNA方式掺入let-7c-5p来调节关键MG基因白介素（IL）-10的表达。此外，功能测定表明，SNHG16通过使let-7c-5p海绵化，抑制Jurkat细胞凋亡并促进细胞增殖。我们的研究将有助于加深对MG调控机制的了解，并可能为MG患者提供新的治疗靶标。萤光素酶报告基因测定证实SNHG16是microRNA（miRNA）let-7c-5p的靶标。随后的实验表明，SNHG16通过以ceRNA方式掺入let-7c-5p来调节关键MG基因白介素（IL）-10的表达。此外，功能测定表明，SNHG16通过使let-7c-5p海绵化，抑制Jurkat细胞凋亡并促进细胞增殖。我们的研究将有助于加深对MG调控机制的了解，并可能为MG患者提供新的治疗靶标。萤光素酶报告基因测定证实SNHG16是microRNA（miRNA）let-7c-5p的靶标。随后的实验表明，SNHG16通过以ceRNA方式掺入let-7c-5p来调节关键MG基因白介素（IL）-10的表达。此外，功能测定表明，SNHG16通过使let-7c-5p海绵化，抑制Jurkat细胞凋亡并促进细胞增殖。我们的研究将有助于加深对MG调控机制的了解，并可能为MG患者提供新的治疗靶标。