The DVL2 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line. This product provides a heterogeneous pool of cells harboring targeted disruptions in the DVL2 gene, enabling loss-of-function studies of DVL2 in a liver cancer context. The polyclonal format retains genetic diversity while ensuring robust knockout of the target gene, suitable for population-level phenotypic analyses without clonal selection biases.
The SK-HEP-1 cell line, originally isolated from ascitic fluid of a liver adenocarcinoma patient, displays a mixed epithelial and endothelial phenotype, reflecting tumor cell plasticity. This makes SK-HEP-1 a valuable model for liver cancer biology, including tumor angiogenesis, metastasis, and epithelial-mesenchymal transition (EMT). It retains key molecular features of hepatocellular carcinoma, facilitating mechanistic studies of oncogenic signaling.
DVL2 encodes a cytoplasmic phosphoprotein that acts as a central scaffold in Wnt signal transduction, bridging Frizzled (FZD1?C10) receptors and downstream effectors. Upon WNT ligand (e.g., WNT3A, WNT5A) binding to FZD/LRP5/6 co-receptors, DVL2 is recruited to the membrane. In the canonical pathway, DVL2 interacts with AXIN1, APC, and GSK3B within the beta-catenin destruction complex, inhibiting GSK3B-mediated phosphorylation and stabilizing beta-catenin. Nuclear beta-catenin partners with TCF/LEF to activate targets like MYC, CCND1, and AXIN2. DVL2 also triggers non-canonical signaling via JNK, RHOA, and RAC1, regulating planar cell polarity and NFAT pathways. It further interfaces with modulators such as DACT1, CK1delta/epsilon, and VANGL1/2.
In the SK-HEP-1 liver adenocarcinoma context, DVL2 sits at the nexus of oncogenic Wnt pathways frequently dysregulated in hepatocellular carcinoma. Knockout of DVL2 in these mixed-morphology cells allows dissection of canonical and non-canonical contributions to proliferation, EMT, and angiogenic signaling. This model is ideal for examining beta-catenin/TCF-dependent transcription, JNK-mediated stress responses, and RHOA/RAC1-driven cytoskeletal changes underlying invasion. It also supports studies on Wnt-dependent drug resistance mechanisms.
This polyclonal DVL2 knockout population supports a broad range of assays: Western blotting and RT-qPCR for DVL2 and targets AXIN2/MYC; TOP/FOP luciferase reporter for beta-catenin/TCF activity; co-immunoprecipitation for protein interactions; migration/invasion assays; and immunofluorescence for beta-catenin localization. The cells are suitable for high-throughput anti-cancer drug screening and resistance studies. For further information, contact Ascent Research.
