The DLG1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma cell line HGC-27, designed for loss-of-function studies of the DLG1 gene (synonym: SAP97). This polyclonal pool, generated by CRISPR/Cas9-mediated gene disruption of DLG1, provides a heterogeneous cell population with targeted disruption of the DLG1 locus, avoiding clonal selection artifacts. The cells serve as a versatile model to investigate the scaffolding functions of DLG1 in epithelial cell polarity, junctional integrity, and signal transduction without the isolation of single-cell clones.
The parental HGC-27 cell line was established from a metastatic lymph node of a gastric adenocarcinoma patient, rendering it an adherent epithelial cell line with high tumorigenic potential. As a widely used model for gastric cancer research, HGC-27 cells retain key features of advanced carcinoma, including invasive capacity and dysregulated signaling networks. This genetic background is particularly suitable for examining the role of cell junction proteins, as the cells form junctional complexes and maintain epithelial characteristics in culture.
DLG1 encodes a membrane-associated guanylate kinase (MAGUK) scaffolding protein that localizes to tight junctions and adherens junctions, where it organizes multiprotein complexes. DLG1 interacts with the APC tumor suppressor, KSR1, and CASK, and is regulated by upstream kinases MARK2 and APC. Through these interactions, DLG1 modulates the Hippo pathway by scaffolding YAP1 and TAZ near LATS1/2 kinases, promoting their phosphorylation and cytoplasmic retention; concurrently, it influences Wnt signaling by binding ??-catenin and LGN. Disruption of DLG1 in this polyclonal knockout population dismantles junctional scaffolds, leading to altered YAP/TAZ nuclear translocation and ??-catenin stabilization, thereby perturbing proliferative and polarity cues.
In the context of HGC-27 gastric carcinoma cells, knockout of DLG1 is expected to compromise epithelial barrier formation, enhance migratory and invasive behaviors, and potentially alter sensitivity to chemotherapeutic agents. The loss of DLG1-mediated scaffolding may promote epithelial-to-mesenchymal transition (EMT)-like changes, consistent with its reported tumor suppressor roles. This model is valuable for dissecting the molecular mechanisms by which DLG1 conveys signals from cell?Ccell contacts to the nucleus, and for evaluating how its absence contributes to gastric cancer progression, metastasis, and drug resistance.
Researchers can employ the DLG1 Knockout HGC-27 Polyclonal Cells for detailed interrogation of Hippo and Wnt signaling using techniques such as Western blotting for phosphorylated YAP (Ser127), immunofluorescence of tight junction markers like ZO-1, and quantitative migration and invasion assays. Proliferation and drug response studies further elucidate DLG1’s role in tumor suppression and chemoresistance. For further technical support or ordering, please contact Ascent Research.
