The DLGAP4 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the DLGAP4 gene in the human gastric carcinoma epithelial cell line HGC-27. This loss-of-function model enables investigation of DLGAP4??s role in scaffolding postsynaptic density proteins and actin cytoskeleton regulation within a gastric cancer context. The polyclonal format provides a heterogeneous pool of gene-disrupted cells that recapitulates diverse mutational outcomes, suitable for functional studies without clonal selection artifacts.
HGC-27 is a widely used human gastric epithelial cell line originally isolated from a lymph node metastasis of a gastric adenocarcinoma patient. These adherent cells exhibit classic epithelial morphology and are established models for dissecting mechanisms of gastric cancer invasion, proliferation, and metastatic progression. Their derivation from a metastatic site renders them particularly relevant for investigating molecular determinants of tumor cell dissemination and actin-dependent motility.
DLGAP4 encodes a scaffold protein that couples DLG4 (PSD-95) and SHANK family proteins to the actin cytoskeleton via cortactin, stabilizing postsynaptic density complexes in neurons. In non-neuronal systems, DLGAP4 interfaces with cell adhesion signaling and actin dynamics. It interacts directly with DLG4, SHANK1?C3, cortactin, and SynGAP, and is regulated by CaMKII- and PKC-mediated phosphorylation. Downstream, DLGAP4 modulates actin cytoskeleton reorganization, AMPA receptor localization, and cell adhesion complex formation, positioning it as a hub linking synaptic organization to cytoskeletal remodeling.
In HGC-27 cells, disruption of DLGAP4 is predicted to perturb actin dynamics and adhesion complexes, potentially altering gastric cancer cell migration, invasion, and signaling. Because DLGAP4 bridges DLG4 and cortactin to filamentous actin (F-actin), its loss may uncouple adhesion receptors from the cytoskeleton, affecting metastatic behavior. This knockout model thus provides a platform to examine how synaptic scaffolding proteins contribute to malignant phenotypes outside the nervous system, with implications for understanding gastric cancer progression and identifying new therapeutic targets.
This DLGAP4 knockout product supports a range of advanced research applications, including functional dissection of synaptic scaffolding proteins in cancer, mechanistic studies of cell adhesion and migration, and drug target validation for neuropsychiatric or gastric cancer therapies. It is compatible with CRISPR-based screening of synaptic gene networks and detailed molecular analyses such as Western blotting, RT-qPCR, immunofluorescence for F-actin and adhesion markers, wound healing migration assays, co-immunoprecipitation of DLG4 and cortactin interactions, and RNA-seq transcriptome profiling. For further information or customized support, please contact Ascent Research.
