The long noncoding RNA MALAT-1 functions as a competing endogenous RNA to regulate MSL2 expression by sponging miR-338-3p in myasthenia gravis.

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.