GRIK3, short for Glutamate ionotropic receptor kainate type subunit 3, is a principal subunit of the kainate-type ionotropic glutamate receptor. It is a predominant excitatory neurotransmitter receptor in the mammalian brain and is involved in normal neurophysiologic processes, such as synaptic potentiation, which is crucial for learning and memory. It also participates in the neuroactive ligand-receptor interaction pathway [1,2,3].

In non-small cell lung cancer (NSCLC), GRIK3 expression is downregulated in cancer tissues compared to paracarcinoma tissues, and its deficiency promotes NSCLC progression by increasing the expression of UBE2C and CDK1, thus activating the Wnt signaling pathway [1]. In gastric cancer (GC), higher GRIK3 expression is associated with poor survival outcomes, and it is an independent prognostic factor related to tumor TNM stage and lymph node metastasis [3]. In breast cancer, GRIK3 promotes epithelial-mesenchymal transition, cell proliferation, and migration by regulating SPDEF/CDH1 signaling [4]. In colorectal cancer, hsa_circ_0038646 promotes cell proliferation and migration via miR-331-3p/GRIK3 axis, and circASXL1 acts as an oncogene in CRC malignant progression by inducing GRIK3 through sponging miR-1205 [5,6].

In conclusion, GRIK3 is important in normal neurophysiologic processes. Its dysregulation is associated with multiple cancers, including NSCLC, GC, breast cancer, and colorectal cancer. Research on GRIK3 in these disease models helps understand its role in cancer progression, potentially providing new prognostic and therapeutic targets.