The DLG1 Knockout Huh-7 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 hepatocellular carcinoma line. Disruption of the DLG1 gene generates a loss-of-function model suitable for investigating the scaffolding protein’s role in epithelial junction signaling. The polyclonal nature minimizes clonal selection artifacts and provides a heterogeneous pool for direct application in diverse biochemical and cell biological assays.
The Huh-7 host line is a well-differentiated epithelial hepatocellular carcinoma model isolated from a human liver tumor. It is widely used in liver cancer biology and hepatitis C virus replication studies due to its retention of hepatocyte features and intact tight junctions. Huh-7 cells express components of the Wnt and Hippo pathways, providing a physiologically relevant background to examine how DLG1 disruption affects tumor-suppressive and oncogenic signaling in hepatic malignancies. Their adherent, junction-forming phenotype facilitates quantitative assays of epithelial barrier function.
DLG1 encodes a multi-domain scaffold protein of the MAGUK family that localizes to cell-cell junctions and organizes signaling complexes governing polarity, adhesion, and proliferation. Upstream regulators include E-cadherin, integrins, Src kinase, and PKC. DLG1 directly interacts with partners such as APC, PTEN, JAM-A, ZO-2, and LATS1/2, thereby influencing ??-catenin transcriptional activity, YAP/TAZ nuclear translocation, and AKT phosphorylation. It thus functions as a critical node coordinating Wnt/??-catenin, Hippo/YAP, and PI3K/AKT pathway outputs at epithelial junctions.
In Huh-7 cells, DLG1 knockout potentially disrupts tight junction architecture and apical-basal polarity, shifting the balance of ??-catenin and YAP/TAZ signaling. Given the roles of these pathways in hepatic tumorigenesis, DLG1 loss may promote a more proliferative, invasive phenotype, undermining contact inhibition and Hippo-mediated growth control. This model thereby enables dissection of how a single junctional scaffold influences epithelial organization and tumor-suppressive mechanisms within a liver cancer context. The polyclonal pool allows assessment of heterogeneous responses.
This knockout cell product supports applications such as mechanistic studies of Wnt?CHippo crosstalk, assessment of tight junction function via transepithelial resistance and permeability assays, and evaluation of cell migration, invasion, and spheroid growth. It is also suited for RNA-seq-based gene expression profiling and drug sensitivity screening to identify DLG1-linked therapeutic vulnerabilities. Standard assays like western blotting for DLG1 and junctional markers, immunofluorescence, and RT-qPCR are directly applicable. For further details, please contact Ascent Research.
