ArticleMolecular carcinogenesis2019
Glutamate Ionotropic Receptor Kainate Type Subunit 3 (GRIK3) promotes epithelial-mesenchymal transition in breast cancer cells by regulating SPDEF/CDH1 signaling.
Article in Molecular carcinogenesis, 2019. 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, 52 citations in OpenAlex.
- Integrating tumor and immune cell transcriptomics to predict immune checkpoint inhibitor primary resistance in metastatic melanoma.Oncoimmunology · 2026Article
- Glutamate Ionotropic Kainate Receptors as Therapeutic Targets in Enzalutamide-Resistant and Neuroendocrine Prostate Cancer.International journal of molecular sciences · 2026Article
- Long non-coding RNA SOCS2-AS1 inhibits gastric cancer progression via the miR-324-3p/GRIK3 axis: a mechanistic study.World journal of surgical oncology · 2026Article
- Aberrant coupling of glutamate and tyrosine kinase receptors enables neuronal control of brain-tumor growth.Neuron · 2025Article
- Leveraging functional annotations to map rare variants associated with Alzheimer disease with gruyere.American journal of human genetics · 2025Article
- Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor.Nature biomedical engineering · 2024Article
- Human pluripotent stem cell-derived kidney organoids reveal tubular epithelial pathobiology of heterozygous HNF1B-associated dysplastic kidney malformations.Stem cell reports · 2024Article
- Article
- spatialHeatmap: visualizing spatial bulk and single-cell assays in anatomical images.NAR genomics and bioinformatics · 2024Article
- Differential gene expression and pathway analysis in growth hormone-secreting pituitary tumors according to granulation pattern.Frontiers in oncology · 2024Article
- Neurotransmitter receptor-related gene signature as potential prognostic and therapeutic biomarkers in colorectal cancer.Frontiers in cell and developmental biology · 2023Article
- GRIK3 deficiency promotes non-small cell lung cancer progression by the regulation of the UBE2C/CDK1/Wnt signaling pathway.American journal of cancer research · 2023Article
- Ligand-Gated Ion Channels as Targets for Treatment and Management of Cancers.Frontiers in physiology · 2022Review
- Involvement of CDK11B-mediated SPDEF ubiquitination and SPDEF-mediated microRNA-448 activation in the oncogenicity and self-renewal of hepatocellular carcinoma stem cells.Cancer gene therapy · 2021Article
- CircASXL1 knockdown represses the progression of colorectal cancer by downregulating GRIK3 expression by sponging miR-1205.World journal of surgical oncology · 2021Article
- TERRA Gene Expression in Gastric Cancer: Role of hTERT.Journal of gastrointestinal cancer · 2021Review
- Identification of the hub genes in gastric cancer through weighted gene co-expression network analysis.PeerJ · 2021Article
- Hsa_circ_0038646 promotes cell proliferation and migration in colorectal cancer via miR-331-3p/GRIK3.Oncology letters · 2020Article
- The long noncoding RNA lncNB1 promotes tumorigenesis by interacting with ribosomal protein RPL35.Nature communications · 2019Article
- Up-regulation of SPC25 promotes breast cancer.Aging · 2019Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate Ionotropic Receptor Kainate Type Subunit 3 (GRIK3) is an important excitatory neurotransmitter receptor that plays a significant role in various neurodegenerative diseases. However, the biological functions of GRIK3 in malignancies are largely unknown because of limited related studies. Here, we primarily reported that the expression of GRIK3 was higher in breast cancer tissues than in adjacent noncancerous tissues. GRIK3 expression was also positively correlated with the prognosis of patients with breast cancer. GRIK3 promoted the proliferation and migration abilities of breast cancer cells and enhanced the growth of orthotopically implanted tumors. Mechanically, GRIK3 influenced a range of signaling pathways and key signal transducers, including two epithelial-mesenchymal transition regulators, SPDEF and CDH1. Heterogenous expression of SPDEF and CDH1 counteracted the migration and invasion abilities, respectively, of breast cancer cells induced by GRIK3. Moreover, overexpression of GRIK3 increased the expression of mesenchymal markers and decreased the expression of epithelial markers, resulting in the translocation of β-catenin into the nucleus and the increased β-catenin transcriptional activity. In conclusion, the present study reported a novel oncogenic role of GRIK3. Meanwhile, GRIK3, as a membrane receptor, may also serve as a potential therapeutic target for the treatment of breast cancer.
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