LncRNA KCNQ1OT1 regulates apoptosis and ECM degradation of NP cells via miR-199a-5p/ACTG1 axis in IDD models

Background: It has been reported that lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) involved in various disease progression. However, the role of KCNQ1OT1 in intervertebral disc degeneration (IDD) and its underlying molecular mechanism remains unclear. Objective: To explore the role of KCNQ1OT1 in IDD progression and its underlying molecular mechanism. Methods: IL-1β (10 ng/mL) treated NP cells for 24 h to induce IDD models i n vitro . The interaction among KCNQ1OT1, miR-199a-5p and ACTG1 was predicted by Starbase bioinformatics and verified by dual-luciferase reporter gene assay and RIP assay. CCK-8 assay was performed to assess cell viability, cell apoptosis was detected by flow cytometry, Western blot and qRT-PCR were performed to examine the level of genes and proteins. Results: Our results illustrated that overexpression of KCNQ1OT1 inhibited NP cells apoptosis and ECM degradation in IDD models. KCNQ1OT1 bound to miR-199a-5p and deregulated miR-199a-5p expression, and KCNQ1OT1 regulated NP cells apoptosis and ECM degradation via miR-199a-5p in IDD models. Furthermore, miR-199a-5p knockdown inhibited NP cells apoptosis and ECM degradation via targeting ACTG1, and the decrease of NP cells apoptosis and ECM degradation induced by miR-199a-5p knockdown was reversed by inhibiting ACTG1 in IDD models. Conclusion: KCNQ1OT1 overexpression inhibited NP cells apoptosis and ECM degradation via miR-199a-5p/ACTG1 axis in IDD models. Our findings illustrated the specific molecular mechanism of KCNQ1OT1 regulating IDD progression.