ArticleOncogene2018
Circadian regulator NR1D2 regulates glioblastoma cell proliferation and motility.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
- Identification of drug candidates against glioblastoma with machine learning and high-throughput screening of heterogeneous cellular models.Digital discovery · 2026Article
- The Potential of Chronotherapy and Nanotherapy-Based Strategies for Glioblastoma Treatment.Pharmaceutics · 2026Review
- Article
- Circadian rhythm in immunotherapy and cellular therapy: impacts on the tumor microenvironment.Acta biochimica et biophysica Sinica · 2026Review
- T Cell Exhaustion and Dendritic Cell-Mediated Tertiary Lymphoid Structures (TLSs) Modulation Affect Response to Neoadjuvant Chemoradiotherapy in Microsatellite Stable Rectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Circadian clock and cancer.Military Medical Research · 2026Review
- Stem Cells Run Like Clockwork for Stroke Therapeutics.Stem cell reviews and reports · 2025Article
- Nuclear receptor subfamily 1 group D member 2 induces chemoresistance in ovarian cancer by regulating ferroptosis and immune infiltration.Discover oncology · 2025Article
- Regulation of Stemness by NR1D2 in Colorectal Cancer.Biomedicines · 2025Article
- Integrating SNP data to reveal the adaptive selection features of goat populations in extreme environments.BMC genomics · 2025Article
- Exploring the interplay between circadian rhythms and obesity: A Boolean network approach to understanding metabolic dysregulation.PloS one · 2025Article
- Unveiling tumor senescence-driven prognostic heterogeneity via MALISS in stage II/III colorectal cancer.Frontiers in immunology · 2025Article
- Unravelling the link between circadian clock genes and brain tumors: From pathological disruptions to potential therapeutic interventions.Frontiers in pharmacology · 2025Review
- Nuclear receptor E75/NR1D2 promotes tumor malignant transformation by integrating Hippo and Notch pathways.The EMBO journal · 2024Article
- A Multi-Omics Study of Epigenetic Changes in Type II Alveolar Cells of A/J Mice Exposed to Environmental Tobacco Smoke.International journal of molecular sciences · 2024Article
- Circadian Clock Gene bmal1 Acts as a Tumor Suppressor Gene in a Mice Model of Human Glioblastoma.Molecular neurobiology · 2024Article
- The interplay between the PI3K/AKT pathway and circadian clock in physiologic and cancer-related pathologic conditions.Cell proliferation · 2024Review
- The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024Review
- A Pilot Urinary Proteome Study Reveals Widespread Influences of Circadian Rhythm Disruption by Sleep Deprivation.Applied biochemistry and biotechnology · 2024Article
- Molecular mechanisms of tumour development in glioblastoma: an emerging role for the circadian clock.NPJ precision oncology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear receptor NR1D2 is originally characterized as the repressor of genes involved in circadian rhythm. Recently, it is documented that NR1D2 is overexpressed in various cancers. However, the pathways and biological functions that NR1D2 involved in cancers remain poorly understood. Here, we reported that NR1D2 was abundant in human glioblastoma (GBM) tissue and cell lines but not primary human astrocytes. Silencing of NR1D2 changed the morphology of GBM cells, inhibited cell proliferation and motility, whereas had no effects on apoptosis. Importantly, based on RNA-seq and ChIP assay, we identified receptor tyrosine kinase AXL as a new transcriptional target of NR1D2 in GBM cells. AXL mediated partially the regulatory effects of NR1D2 on PI3K/AKT axis and promoted proliferation, migration, and invasion of GBM cells. Besides, NR1D2 knockdown remarkably impaired the maturation of focal adhesion and assembly of F-actin, along with downregulated p-FAK, and proteins involved in actin nucleation and polymerization (p-Rac1/Cdc42, WAVE and PFN2). Moreover, NR1D2 had more targets other than AXL to regulate epithelial-to-mesenchymal transition and cell motility in GBM cells. Altogether, our findings uncover a GBM-promoting role of NR1D2 and provide the rationale for targeting NR1D2 as a potential therapeutic approach.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.