The DLG5 Knockout SK-HEP-1 Polyclonal Cells product comprises a heterogeneous pool of SK-HEP-1 human hepatocellular carcinoma cells that have undergone CRISPR/Cas9?mediated disruption of the DLG5 gene. This polyclonal knockout population provides a loss?of?function model for interrogating DLG5?dependent cellular processes while avoiding clonal selection biases and preserving the genetic heterogeneity typical of tumor cell populations.
The parental SK?HEP?1 cell line is derived from a human hepatic adenocarcinoma and exhibits an epithelial morphology. It is widely used in hepatocellular carcinoma (HCC) research to study signaling networks, tumor progression, and drug responses. These cells retain functional Hippo, Wnt, and other oncogenic pathways, making them a relevant platform for investigating HCC biology.
DLG5 is a membrane?associated guanylate kinase scaffold protein that regulates epithelial polarity and tight junction assembly. Activated by cell?Ccell contacts and upstream signals such as WNT3A, RAC1, and CDC42, DLG5 anchors junctional complexes through direct interactions with TJP1 (ZO?1), occludin (OCLN), and claudin?1 (CLDN1). Simultaneously, DLG5 modulates Hippo signaling by binding to AMOT and the polarity proteins PARD3 and CRB3, which influence the MST1/2?CLATS1/2 kinase cascade, ultimately controlling YAP/TAZ nuclear localization and transcriptional output. Through its association with ???catenin (CTNNB1), DLG5 also intersects the Wnt pathway. Consequently, disruption of DLG5 compromises tight junction integrity, abolishes cell polarity, and promotes YAP/TAZ?mediated transcription of pro?proliferative and pro?migratory genes.
In the SK?HEP?1 hepatocellular carcinoma background, DLG5 knockout serves as a valuable model to examine how loss of this scaffold protein drives malignant behavior. Abrogation of DLG5 is predicted to destabilize intercellular junctions, weaken barrier function, and aberrantly activate YAP/TAZ?dependent gene programs that enhance proliferation, migration, and invasion??hallmarks of aggressive HCC in which DLG5 is frequently downregulated.
This polyclonal knockout product enables diverse research applications. Investigators can study HCC progression through migration/invasion transwell assays, proliferation measurements (BrdU/EdU incorporation), and apoptosis detection by flow cytometry. Tight junction functionality can be assessed by immunofluorescence for TJP1, CLDN1, and OCLN, together with TEER measurements. Hippo pathway activity is measurable via YAP/TAZ transcriptional reporter assays or Western blotting for phosphorylated MST1/2 and LATS1/2. The model also supports drug sensitivity testing (e.g., sorafenib) and transcriptomic analyses by RNA?seq. For further details, please contact Ascent Research.
