The DVL2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HeLa cells, featuring targeted disruption of the DVL2 gene. As a scaffold in Wnt signaling, DVL2 is essential for ??-catenin stabilization and planar cell polarity. This polyclonal format enables pooled functional studies, avoiding clonal artifacts and ensuring robust representation of knockout effects. The product is a versatile tool for investigating Wnt pathway function in a cancer-relevant epithelial background.
HeLa cells are a cervical adenocarcinoma line positive for HPV18, with E6- and E7-mediated inactivation of p53 and Rb, respectively. The line is highly aneuploid and widely used in cancer biology and virology. These genetic alterations create a hyperproliferative milieu ideal for studying oncogenic pathways. HeLa’s robust growth and transfectability facilitate CRISPR editing, allowing precise dissection of gene function in malignant epithelium.
DVL2 acts as a phosphoprotein scaffold that bridges Frizzled receptors and LRP5/6 to downstream effectors. Upon Wnt3a stimulation, DVL2 is phosphorylated by CK1?? and CK2, recruiting AXIN, GSK3??, and CK1 to dissociate the destruction complex. This stabilizes ??-catenin, which translocates to the nucleus and co-activates TCF/LEF transcription factors, inducing targets such as c-MYC and CCND1. DVL2 also mediates non-canonical planar cell polarity via interactions with VANGL and PRICKLE, regulating RAC1 and RHOA GTPases to control cytoskeletal dynamics.
In HeLa cells, DVL2 knockout disrupts canonical Wnt transcriptional responses and may impair PCP-driven migration. The abrogation of ??-catenin-dependent transcription can be quantified by TOP/FOP reporter assays, while loss of DVL2 impacts migration and invasion. This model thus reveals how oncogenic Wnt signaling cooperates with HPV-induced transformation to maintain malignant phenotypes, offering a platform for evaluating Wnt-targeted therapies.
Key applications include Western blotting for ??-catenin and phospho-DVL2, RT-qPCR of Wnt targets, immunofluorescence localization, and co-immunoprecipitation of DVL2 complexes. The knockout cells are suitable for drug screening, cell migration assays, and flow cytometric cell cycle analysis. Researchers can leverage this model to dissect DVL2-dependent mechanisms in cancer. For inquiries, please contact Ascent Research.
