ArticleJournal of molecular neuroscience : MN2022
Stat3-Induced lncRNA Kcnq1ot1 Regulates the Apoptosis of Neuronal Cells in Spinal Cord Injury.
Article in Journal of molecular neuroscience : MN, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function.Cell proliferation · 2025Article
- An Unanticipated Modulation of Cyclin-Dependent Kinase Inhibitors: The Role of Long Non-Coding RNAs.Cells · 2022Review
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Authors and funding
5 authors at 3 institutions in 1 country.
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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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