ArticleFrontiers in cell and developmental biology2021
NLGN3 Upregulates Expression of ADAM10 to Promote the Cleavage of NLGN3
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- The malignant synapse: architecture, signal integration, and therapeutic vulnerabilities in glioma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance.Biology · 2026Review
- Neural regulation of tumor progression: implications for hepatocellular carcinoma.Frontiers in immunology · 2026Review
- Review of glioblastoma and systemic comorbidities.Frontiers in oncology · 2026Review
- The Neuro-Melanoma Singularity: Convergent Evolution of Neural and Melanocytic Networks in Brain Metastatic Adaptation.Biomolecules · 2025Review
- ADAM10 Knockout from Human Glioblastoma and Colon Cancer Cells Modulates Diverse Signalling Networks and Inhibits Tumour Growth In Vivo.International journal of molecular sciences · 2025Article
- Therapeutic approaches for targeting the pediatric brain tumor microenvironment.Drug delivery and translational research · 2025Review
- Review
- Oligodendroglioma: Advances in Molecular Mechanisms and Immunotherapeutic Strategies.Biomedicines · 2025Review
- Breaking Down Glioma-Microenvironment Crosstalk.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- Neural Influences on Tumor Progression Within the Central Nervous System.CNS neuroscience & therapeutics · 2024Review
- Dysregulated gene subnetworks in breast invasive carcinoma reveal novel tumor suppressor genes.Scientific reports · 2024Article
- Molecular diversity in isocitrate dehydrogenase-wild-type glioblastoma.Brain communications · 2024Review
- Neuromodulation for Brain Tumors: Myth or Reality? A Narrative Review.International journal of molecular sciences · 2023Review
- Neuropilin-1 Knockout and Rescue Confirms Its Role to Promote Metastasis in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Glioma‑neuronal interactions in tumor progression: Mechanism, therapeutic strategies and perspectives (Review).International journal of oncology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuron derived synaptic adhesion molecular neuroligin-3 (NLGN3) plays an important role in glioma growth. While the role of autocrine NLGN3 in glioma has not been well-studied. The expression of NLGN3 in glioma was detected using immunohistochemistry. We further explored its function and regulatory mechanism in U251 and U87 cells with high expression of NLGN3. Knockdown of endogenous NLGN3 significantly reduced the proliferation, migration, and invasion of glioma cells and down-regulated the activity of the PI3K-AKT, ERK1/2, and LYN signaling pathways. In comparison, overexpression of NLGN3 yielded opposite results. Our results further demonstrate that LYN functions as a feedback mechanism to promote NLGN3 cleavage. This feedback regulation was achieved by upregulating the ADAM10 sheddase responsible for NLGN3 cleavage. Inhibition of ADAM10 suppressed the proliferation, migration, and invasion of glioma cells; oppositely, the expression of ADAM10 was correlated with a higher likelihood of lower grade glioma (LGG) in the brain. Our study demonstrates that glioma-derived NLGN3 promotes glioma progression by upregulating activity of LYN and ADAM10, which in turn promote NLGN3 cleavage to form a positive feedback loop. This pathway may open a potential therapeutic window for the treatment of human glioma.
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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 Socratic graph.