The DVL2 Knockout HT29 Polyclonal Cells are a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population that carries a targeted disruption of the DVL2 gene, encoding the dishevelled segment polarity protein 2. This model provides a powerful tool for investigating DVL2-dependent signaling pathways without the need for transient knockdown approaches, enabling robust loss-of-function studies in a genetically defined background. The polyclonal nature of the population captures the heterogeneity of CRISPR-induced edits, reflecting a pooled knockout profile that can be used directly in functional assays or further enriched for specific experimental needs.
The host cell line HT29 is derived from a human colorectal adenocarcinoma, presenting an epithelial morphology and retaining the ability to undergo differentiation into an enterocyte-like phenotype under appropriate induction conditions. HT29 cells are widely employed as a model system for intestinal epithelial biology and colorectal cancer, offering a relevant context for studying oncogenic signaling, cell polarity, and tumor cell behavior. Their robust growth and well-characterized signaling networks make them an ideal chassis for gene-editing applications.
DVL2 functions as a central cytoplasmic mediator of Wnt signal transduction, acting downstream of Frizzled receptors and LRP5/6 co-receptors upon stimulation by Wnt ligands such as Wnt1 and Wnt3a. In the canonical Wnt/??-catenin pathway, DVL2 interacts with AXIN, GSK3??, and CK1 to inhibit the ??-catenin destruction complex, promoting ??-catenin stabilization, nuclear translocation, and activation of TCF/LEF transcription factors that drive expression of target genes including MYC and CCND1. Beyond the canonical axis, DVL2 activates the non-canonical Wnt/planar cell polarity (PCP) pathway through RhoA and ROCK, regulating actin cytoskeleton dynamics, and engages the Wnt/Ca2+ pathway via JNK. DVL2 also forms homomeric and heteromeric complexes via its DIX domain and interacts with Van Gogh-like (VANGL) proteins to coordinate planar polarity signaling events.
In HT29 colorectal cancer cells, DVL2 is positioned at a critical node connecting Wnt signaling to malignant phenotypes, including uncontrolled proliferation, epithelial?Cmesenchymal transition, and invasive capacity. Loss of DVL2 in this cellular context disrupts both ??-catenin?Cdriven transcription and PCP-mediated cytoskeletal rearrangements, thereby attenuating tumorigenic properties. This knockout model thus enables researchers to dissect the contribution of DVL2 to colorectal cancer pathogenesis, evaluate its role in maintaining stemness features, and explore its crosstalk with other signaling modules that drive tumor progression and metastatic dissemination.
The DVL2 Knockout HT29 Polyclonal Cells are suitable for a broad range of experimental workflows, including Western blotting for ??-catenin and phospho-DVL2, RT-qPCR quantification of Wnt target genes (MYC, CCND1), TOP/FOP Flash reporter assays for ??-catenin transcriptional activity, and immunofluorescence analysis of ??-catenin subcellular localization. Functional studies can incorporate cell proliferation (MTT/BrdU), Transwell migration and invasion assays, colony formation, and drug sensitivity testing with Wnt pathway inhibitors such as ICG-001 and LGK-974. These cells also support tumorigenicity assessments in xenograft models. For further details and technical support, please contact Ascent Research.
