ArticleCurrent molecular medicine2025
ADGRL4 Promotes Cell Growth, Aggressiveness, EMT, and Angiogenesis in Neuroblastoma via Activation of ERK/STAT3 Pathway.
Article in Current molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- aGPCR-HEK: A Stable High-Expression Inducible Mammalian Cell Expression System for Adhesion GPCR Structural Biology Applications.Bio-protocol · 2026Article
- Purification of the Active-State G Protein-Coupled Receptor ADGRL4 for Cryo-Electron Microscopy Using a Modular Tag System and a Tethered mini-GBio-protocol · 2026Article
- ADGRD1 promotes bladder cancer progression and angiogenesis via the PI3K/AKT/mTOR-mediated pro-angiogenic secretome.Frontiers in oncology · 2026Article
- Structure of the GNature communications · 2025Article
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
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Abstract
backgroundNeuroblastoma (NB) is one of the most common pediatric solid tumors. Emerging evidence has indicated that ADGRL4 can act as a master regulator of tumor progression. In addition, it is well documented that the ERK/STAT3 signaling pathway can promote the proliferation, EMT, angiogenesis, and metastasis in tumors. The current study was formulated to elucidate the exact role of ADGRL4 in the malignant behaviors of NB cells and to investigate the intrinsic mechanism.
methodsIn this work, expression differences of ADGRL4 in human NB cell lines and HUVECs were assessed via RT-qPCR and western blot analysis. For functional experiments, sh-ADGRL4 was transfected into SK-N-SH cells to generate ADGRL4 knockdown stable cell line. Moreover, ADGRL4 knockdown stable SK-N-SH cells were treated with LM22B-10 (an ERK activator) for rescue experiments. CCK-8, colony formation, would healing, and transwell assays determined NB cell growth, migration, and invasion. Meanwhile, proliferation-, metastasis- and EMT- associated proteins were also detected. Additionally, a tube formation assay was employed to evaluate
resultsData showed notably upregulated ADGRL4 in NB cells, especially in SK-NSH cells. ADGRL4 knockdown inhibited NB cell growth, migration, invasion, EMT, and
conclusionTo conclude, the downregulation of ADGRL4 may inhibit cell growth, aggressiveness, EMT, and angiogenesis in NB by inactivating the ERK/STAT3 signaling pathway.
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