The DLG3 Knockout A-549 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, engineered for loss-of-function studies of the DLG3 gene. This knockout model provides a genetically defined system to investigate the roles of DLG3 in cellular signaling and cancer biology without relying on transient suppression methods, thereby enabling stable, long-term experimental analyses.
The parental A-549 cell line, derived from a 58-year-old Caucasian male, is a widely used epithelial model of human lung adenocarcinoma displaying alveolar basal morphology. These cells grow robustly in standard culture and are suitable for high-throughput screening, migration assays, and biochemical analyses. The A-549 background features activated KRAS signaling, which intersects with DLG3-related pathways.
DLG3 (discs large MAGUK scaffold protein 3) is a membrane-associated guanylate kinase (MAGUK) scaffold protein that organizes multimeric signaling complexes at the plasma membrane. DLG3 is activated by NMDA receptor activation and CaMKII, and it interacts directly with NMDA and AMPA receptor subunits, CaMKII, PTEN, APC, DLG1, and DLG4. Through these interactions, DLG3 regulates downstream targets such as AKT phosphorylation and ERK1/2 activation, thereby modulating key signaling cascades including the PTEN/AKT and Wnt/??-catenin pathways. In the context of A-549 cells, DLG3 may influence tumor-suppressive mechanisms through its scaffolding of PTEN, a negative regulator of the PI3K/AKT pathway, and through its interaction with APC, a component of the ??-catenin destruction complex.
Disruption of DLG3 in A-549 knockout cells is expected to perturb the organization of postsynaptic-like signaling complexes, leading to altered AKT and ERK signaling dynamics, changes in cell polarity, and modified cell proliferation and migration behaviors. As A-549 cells express both NMDA and AMPA receptor subunits, this knockout model allows investigation of neuronal scaffold protein functions in a non-neuronal cancer context, offering insights into the cross-talk between synaptic scaffolding and oncogenic pathways. This polyclonal population, generated by CRISPR/Cas9-mediated gene disruption, provides a heterogeneous pool of edited cells suitable for studying population-level functional responses, avoiding clonal selection biases.
Researchers can employ this DLG3 knockout product in a variety of assays including Western blotting and RT-qPCR to confirm target protein depletion and transcript loss, immunofluorescence to assess changes in cell polarity and junctional organization, and functional assays such as wound healing and transwell migration to evaluate migratory capacity. Proliferation can be analyzed via MTT or BrdU incorporation, while phospho-AKT and ERK1/2 levels can be monitored to assess pathway activity. Co-immunoprecipitation experiments using these cells can map DLG3-associated interactomes in lung cancer. The model is ideal for lung cancer research, tumor suppressor gene studies, drug target discovery, and mechanistic investigations into cell polarity and migration. For additional product details or technical support, please contact Ascent Research.
