The DMD Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells. This model features targeted disruption of the DMD gene, encoding dystrophin, a cytoskeletal protein that links the actin cytoskeleton to the extracellular matrix via the dystrophin-glycoprotein complex (DGC). The polyclonal format provides a heterogeneous loss-of-function model without clonal artifacts.
HT29 cells, established from a primary colorectal adenocarcinoma, exhibit adherent epithelial morphology and are widely used in cancer research and drug screening. They can differentiate into intestinal epithelial-like monolayers with barrier properties, making them a robust system for studying colorectal cancer biology and intestinal differentiation.
Dystrophin scaffolds intracellular F-actin to ??-dystroglycan, anchoring cells to the matrix and maintaining sarcolemma integrity. The DGC also includes sarcoglycans, syntrophins, dystrobrevin, and nNOS. DMD signaling is regulated by MyoD, SP1, YY1, mechanical stretch, calcium influx, and NF-??B, and it influences downstream ??-catenin stabilization, FAK activity, and MAPK/ERK pathways. DMD knockout disrupts DGC assembly, impairing cell adhesion and altering Wnt/??-catenin and integrin signaling, potentially affecting migration and tumorigenic potential.
In HT29 cells, dystrophin loss may compromise epithelial adhesion and polarization, impacting colorectal cancer metastasis. This model enables dissection of DMD??s role in ??-catenin localization, focal adhesion dynamics, and ERK-mediated proliferation. It also allows study of dystrophin-dependent apoptosis regulators and calcium homeostasis within the intestinal epithelium.
Key applications include western blotting, immunofluorescence for DGC components, adhesion and migration assays, ??-catenin localization, RNA-seq, flow cytometry, and co-immunoprecipitation. These cells support drug screening for dystrophin compensators, modeling muscular dystrophy in an epithelial context, and analyzing DMD-related signaling. For further details, please contact Ascent Research.
