ArticleCell death & disease2023
Super-enhancer-driven lncRNA LIMD1-AS1 activated by CDK7 promotes glioma progression.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- Associations between migrasome-related genes and long non-coding rnas in glioma and their prognostic relevance to the tumor microenvironment.IBRO neuroscience reports · 2026Article
- Article
- Overexpression of Circular RNA circTTN Promotes Ferroptosis in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2026Article
- Disrupting MED8-dependent epigenetic reprogramming augments avapritinib sensitivity in PDGFRA-driven glioma.Journal of experimental & clinical cancer research : CR · 2026Article
- Elastic enhancer network tunes equilibrium thermodynamics of liquid liquid phase separation in super enhancers.iScience · 2026Article
- Targeting super-enhancer-driven SKIL transcription by CDK7 inhibitor THZ1 to suppress gastric cancer progression.Journal of translational medicine · 2026Article
- The Clinical Diagnostic Value of the Super-enhancer-associated Long Noncoding RNA RP11-803D5.4 and AC005592.2 in Colorectal Cancer.Current medicinal chemistry · 2026Article
- Co-activation of the super-enhancer complex SOX2 and HDAC1 confers temozolomide resistance by promoting PDGFB transcription in glioblastoma.Neuro-oncology · 2026Article
- The Role of LncRNAs in Radio- and Chemoresistance of Glioblastoma: Prognostic or Therapeutic?Current oncology (Toronto, Ont.) · 2025Review
- SMAD3 and p300 complex scaffolding by long non-coding RNA LIMD1-AS1 promotes TGF-β-induced breast cancer cell plasticity.Nucleic acids research · 2025Article
- Review
- Super-enhancers in tumors: unraveling recent advances in their role in Oncogenesis and the emergence of targeted therapies.Journal of translational medicine · 2025Review
- Super-enhancer inhibitors THZ2 and JQ1 reverse temozolomide resistance in glioblastoma by suppressing SE-driven SOX9 expression.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- The role of super-enhancer-driven lncRNAs in cancer.Computational and structural biotechnology journal · 2025Review
- The multiple functions and mechanisms of long non-coding RNAs in regulating breast cancer progression.Frontiers in pharmacology · 2025Review
- SE-lncRNAs in Cancer: Classification, Subcellular Localisation, Function and Corresponding TFs.Journal of cellular and molecular medicine · 2024Review
- Super-enhancer-driven LIF promotes the mesenchymal transition in glioblastoma by activating ITGB2 signaling feedback in microglia.Neuro-oncology · 2024Article
- The pathogenesis mechanism and potential clinical value of lncRNA in gliomas.Discover oncology · 2024Review
- CCAT1 lncRNA is chromatin-retained and post-transcriptionally spliced.Histochemistry and cell biology · 2024Article
- Super enhancer lncRNAs: a novel hallmark in cancer.Cell communication and signaling : CCS · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) are tissue-specific expression patterns and dysregulated in cancer. How they are regulated still needs to be determined. We aimed to investigate the functions of glioma-specific lncRNA LIMD1-AS1 activated by super-enhancer (SE) and identify the potential mechanisms. In this paper, we identified a SE-driven lncRNA, LIMD1-AS1, which is expressed at significantly higher levels in glioma than in normal brain tissue. High LIMD1-AS1 levels were significantly associated with a shorter survival time of glioma patients. LIMD1-AS1 overexpression significantly enhanced glioma cells proliferation, colony formation, migration, and invasion, whereas LIMD1-AS1 knockdown inhibited their proliferation, colony formation, migration, and invasion, and the xenograft tumor growth of glioma cells in vivo. Mechanically, inhibition of CDK7 significantly attenuates MED1 recruitment to the super-enhancer of LIMD1-AS1 and then decreases the expression of LIMD1-AS1. Most importantly, LIMD1-AS1 could directly bind to HSPA5, leading to the activation of interferon signaling. Our findings support the idea that CDK7 mediated-epigenetically activation of LIMD1-AS1 plays a crucial role in glioma progression and provides a promising therapeutic approach for patients with glioma.
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