The DLG1 Knockout 786-O Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of 786-O cells with targeted disruption of the DLG1 gene. This loss-of-function model enables investigation of DLG1-dependent signaling and tumor-suppressive functions in a renal cell carcinoma context.
The 786-O host cell line is a well-established human clear cell renal cell carcinoma (ccRCC) model derived from a primary renal adenocarcinoma. These cells harbor a von Hippel-Lindau (VHL) gene mutation and exhibit epithelial morphology, making them highly relevant for studying ccRCC biology, including hypoxia signaling and tumor progression.
DLG1 (Discs Large Homolog 1) encodes a membrane-associated guanylate kinase (MAGUK) scaffold protein that orchestrates multiprotein complexes at cell-cell junctions. It directly interacts with APC, PTEN, LIN7, CASK, and KIF1B. DLG1 integrates upstream signals from Wnt ligands, mechanical stretch, and kinases such as CaMKII, CDK5, and LKB1 to regulate downstream effectors including ??-catenin, YAP/TAZ, Akt, and tight junction components ZO-1, occludin, and claudins. In the Wnt/??-catenin pathway, DLG1 associates with APC and ??-catenin, modulating ??-catenin nuclear translocation and TCF/LEF-mediated transcription; disruption of DLG1 can lead to Wnt pathway hyperactivation. Concurrently, DLG1 participates in Hippo pathway signaling by interacting with components such as MST1/2 and LATS1/2, thereby influencing YAP/TAZ phosphorylation and nuclear localization. Through these scaffold functions, DLG1 maintains apical-basal polarity and junctional integrity.
In the 786-O ccRCC model, CRISPR/Cas9-mediated knockout of DLG1 is expected to perturb tight junction assembly and cell polarity, promoting epithelial-mesenchymal transition (EMT) and invasive behavior. Loss of DLG1 likely enhances ??-catenin and YAP/TAZ transcriptional activity, driving proliferation and migration. This knockout thus serves as a powerful system to dissect the tumor-suppressive role of DLG1 in renal cancer and to explore crosstalk between Wnt and Hippo pathways in a VHL-deficient background.
Researchers can employ this polyclonal DLG1 knockout cell population in diverse assays, including Western blotting to assess ??-catenin and YAP/TAZ levels, immunofluorescence for junctional markers, RT-qPCR for Wnt target genes, and migration/invasion assays to evaluate metastatic potential. Co-immunoprecipitation enables study of DLG1 interaction partners such as APC and PTEN, while RNA-seq provides global transcriptional profiling. Drug sensitivity assays can elucidate the role of DLG1 in therapeutic response. For further information, please contact Ascent Research.
