Abstract
Emerging evidence validates the vital roles of long noncoding RNAs (lncRNAs) in spinal cord injury (SCI), which attracts great attention. In the present study, our study investigated the function and in-depth mechanism of lncRNA Kcnq1 overlapping transcript 1 (Kcnq1ot1) in SCI. Results indicated that lncRNA Kcnq1ot1 expression upregulated in the hypoxia-administered neuronal cells (PC12 cells) and SCI rat models. Moreover, transcription factor signal transducer and activator of transcription 3 (Stat3) accelerated the transcriptional enrichment of Kcnq1ot1 in SCI cellular model. Functional experiments demonstrated that Kcnq1ot1 knockdown repressed the apoptosis of neuronal cells. Mechanistically, Kcnq1ot1 recruited EZH2 to the promoter region of p27 to repress its transcription. Taken together, our results indicate that Stat3-induced lncRNA Kcnq1ot1 regulates the apoptosis in SCI through epigenetically silencing p27, contributing to novel therapeutic target for SCI.
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