DVL3 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population in which the DVL3 gene is disrupted to create a loss-of-function model. These polyclonal knockout cells are derived from the SK-HEP-1 human hepatic adenocarcinoma line and provide a heterogeneous but genetically defined cell pool for investigating DVL3-dependent signaling. By circumventing single-cell clonal selection, this format offers a practical tool for cancer biologists studying Wnt pathway dynamics in a liver cancer context.
The SK-HEP-1 host cell line was isolated from the ascitic fluid of a 52-year-old male diagnosed with liver adenocarcinoma. These cells exhibit both epithelial and mesenchymal characteristics, rendering them particularly apt for dissecting mechanisms of hepatocellular carcinoma progression, including tumor cell motility and epithelial-mesenchymal transition. As a well-established model in liver cancer research, SK-HEP-1 cells enable meaningful interrogation of oncogenic pathways in a cell-autonomous setting.
DVL3 encodes a cytoplasmic scaffold protein that transduces Wnt signals from Frizzled receptors. Upon binding of WNT3A or WNT5A to FZD?CLRP5/6 or FZD?CROR2 co-receptor complexes, DVL3 inhibits the AXIN/GSK3??/APC/CK1 destruction complex, stabilizing ??-catenin for nuclear translocation and TCF/LEF-mediated transcription of MYC, CCND1, and AXIN2. DVL3 also activates non-canonical pathways via JNK and RHO GTPases, affecting planar cell polarity and calcium signaling. Interacting proteins include AXIN, GSK3??, CK1, DACT, and NKD, positioning DVL3 at a central node in Wnt signal integration.
In hepatocellular carcinoma, DVL3 is often implicated in the aberrant activation of Wnt signaling that promotes tumor growth and metastasis. The SK-HEP-1 knockout model thus enables researchers to dissect DVL3’s specific contributions to ??-catenin-dependent proliferation, cell survival, and epithelial-mesenchymal plasticity. By comparing knockout and wild-type cells, one can assess how loss of DVL3 reprograms Wnt target gene expression and disrupts oncogenic signaling networks intrinsic to liver cancer cells.
This polyclonal DVL3 knockout cell product is suitable for a wide array of assays, including Western blot detection of DVL3 and ??-catenin, TOP/FOP flash reporter assays to gauge TCF/LEF activity, and RT-qPCR quantification of MYC and CCND1 transcripts. Immunofluorescence can monitor ??-catenin nuclear localization, while proliferation and transwell migration assays evaluate functional consequences. Co-immunoprecipitation experiments probe DVL3 interactions with destruction complex components, and phospho-signaling arrays reveal pathway dependencies. For additional information or to request a quotation, please contact Ascent Research.
