Department of Neurology, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China.
Department of Neurology, Peking Union Medical College Hospital, Beijing, China.
J Cell Biochem. 2019 Apr;120(4):5542-5550. doi: 10.1002/jcb.27838. Epub 2018 Oct 26.
Myasthenia gravis (MG) is a cell-dependent autoimmune disease commonly associated with thymic pathology. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) has been associated with gene regulation and alternative splicing. It has shown relationship with proliferation, apoptosis, migration, and invasion. In this study, we found that MALAT-1 expression was downregulated in MG. The level of the miR-338-3p was increased in peripheral blood mononuclear cells from MG patients compared with those from control subjects. MALAT-1 competed for binding to miR-338-3p with male-specific lethal 2 (MSL2) in luciferase reporter assays. We confirmed the MALAT-1-miR-338-3p-MSL2 interaction network in MG in vitro. Thus, MALAT-1 directly induced MSL2 expression in MG by acting as a competing endogenous RNA for miR-338-3p, suggesting that it may serve as a therapeutic target for MG treatment.
重症肌无力（MG）是一种以胸腺病理学为特征的细胞依赖性自身免疫性疾病。转移相关肺腺癌转录物 1（MALAT-1）与基因调控和可变剪接有关。它与增殖、凋亡、迁移和侵袭有关。在这项研究中，我们发现 MG 中 MALAT-1 的表达下调。与对照组相比，MG 患者外周血单个核细胞中 miR-338-3p 的水平增加。在荧光素酶报告实验中，MALAT-1 与雄性特异性致死 2（MSL2）竞争与 miR-338-3p 的结合。我们在体外证实了 MG 中的 MALAT-1-miR-338-3p-MSL2 相互作用网络。因此，MALAT-1 通过作为 miR-338-3p 的竞争性内源性 RNA 直接诱导 MG 中的 MSL2 表达，表明它可能作为 MG 治疗的治疗靶点。
