ArticleCancer cell2016
Inhibition of Dopamine Receptor D4 Impedes Autophagic Flux, Proliferation, and Survival of Glioblastoma Stem Cells.
Article in Cancer cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
145 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Dopamine D1-like and Angiotensin II Type 1 Receptors Counter-Regulate Autophagy and Cell Proliferation in Rat Embryonic Thoracic Vascular Smooth Muscle Cells.International journal of molecular sciences · 2026Article
- Spiramide and Hydroquinidine Inhibit Proliferation and Migration While Promoting Apoptosis and Oxidative Stress in Neuroblastoma Cells.International journal of molecular sciences · 2026Article
- From Antipsychotic to Antitumor Agent: Cariprazine Suppresses Glioblastoma via D2/D3-ARRB2 Axis Modulation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Spirohydantoin derivatives exert dopamine DScientific reports · 2026Article
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Bidirectional crosstalk between the nervous system and the tumour microenvironment: mechanisms, feedback loops and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Neural regulation of tumor progression: implications for hepatocellular carcinoma.Frontiers in immunology · 2026Review
- Decoding autophagy in neuro-tumor crosstalk: from underlying mechanisms to translational opportunities.Theranostics · 2026Review
- PDGFRβ in Stem Cell Microenvironments: Cross-Tissue Evidence and Hypotheses for the Limbal Stem Cell Niche.Stem cells international · 2026Review
- Neuron-Glioma Synapses in Tumor Progression.Biomedicines · 2025Review
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- The molecular footprint of the serotoninergic system in human glioblastoma cells.Journal of molecular histology · 2025Article
- Neural Vulnerabilities in Glioblastoma: Rethinking Therapy Through Neuroactive Drug Repurposing.Brain tumor research and treatment · 2025Review
- Cholinergic neuronal activity promotes diffuse midline glioma growth through muscarinic signaling.Cell · 2025Article
- Advances in the treatment of malignant tumors with neurological drugs.Discover oncology · 2025Review
- L2S2: chemical perturbation and CRISPR KO LINCS L1000 signature search engine.Nucleic acids research · 2025Article
- Cancer and neurotransmitter receptors.Chinese medical journal · 2025Review
- Novel Potent and Selective Dopamine D4 Receptor Piperidine Antagonists as Potential Alternatives for the Treatment of Glioblastoma.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Distinct Transcriptomic Profiles of Cultured Anterior and Posterior Populations of Human Infant Scleral Fibroblasts: Including Dopamine Receptors.Investigative ophthalmology & visual science · 2025Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastomas (GBM) grow in a rich neurochemical milieu, but the impact of neurochemicals on GBM growth is largely unexplored. We interrogated 680 neurochemical compounds in patient-derived GBM neural stem cells (GNS) to determine the effects on proliferation and survival. Compounds that modulate dopaminergic, serotonergic, and cholinergic signaling pathways selectively affected GNS growth. In particular, dopamine receptor D4 (DRD4) antagonists selectively inhibited GNS growth and promoted differentiation of normal neural stem cells. DRD4 antagonists inhibited the downstream effectors PDGFRβ, ERK1/2, and mTOR and disrupted the autophagy-lysosomal pathway, leading to accumulation of autophagic vacuoles followed by G0/G1 arrest and apoptosis. These results demonstrate a role for neurochemical pathways in governing GBM stem cell proliferation and suggest therapeutic approaches for GBM.
Indexed as
Identifiers
What OpenQuestion holds
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.