DOCK4 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human Huh-7 hepatocellular carcinoma cell line. This product comprises a heterogeneous pool of cells carrying targeted disruptions in the DOCK4 gene, providing a loss-of-function model without clonal isolation. The polyclonal format preserves genetic variability and is well-suited for pooled functional assays, enabling robust assessment of DOCK4-dependent phenotypes in a mixed population context.
The Huh-7 cell line, established in 1982 from a liver tumor of a 57-year-old Japanese male, is a well-characterized model of hepatocellular carcinoma. These epithelial cells maintain key features of liver cancer, including malignant growth properties and relevant signaling pathway activities. The Huh-7 background is extensively used to study hepatocarcinogenesis, drug metabolism, and therapeutic responses, making it a suitable host for interrogating the role of DOCK4 in liver cancer biology.
DOCK4 encodes a guanine nucleotide exchange factor that specifically activates the small GTPases Rac1 and Cdc42. DOCK4 is recruited and activated by binding to the adaptor protein ELMO and ??-catenin, integrating Wnt/??-catenin signals with cytoskeletal dynamics. Upstream, DOCK4 is regulated by Wnt ligands such as Wnt3a and growth factor receptors, while downstream it promotes Rac1/Cdc42-mediated signaling cascades including PAK kinase activation and WAVE complex assembly, ultimately driving actin polymerization and cellular processes like migration and adhesion. DOCK4 also participates in adherens junction maintenance through its interaction with ??-catenin.
In the Huh-7 hepatocellular carcinoma model, DOCK4 disruption impairs key oncogenic properties. DOCK4 loss-of-function studies in these cells allow direct investigation of the gene’s contribution to liver cancer cell migration, invasion, and Wnt/??-catenin-driven transcriptional programs. Since DOCK4 is implicated in cancer progression, including colorectal and liver cancers, this knockout model provides a physiologically relevant system to examine tumor cell behavior and the molecular mechanisms underlying DOCK4-dependent tumorigenesis and drug resistance.
Typical applications include western blot confirmation of DOCK4 knockdown, Rac1 activation pull-downs to assess GTPase activity, transwell migration and invasion assays, and immunofluorescence staining for F-actin to visualize cytoskeletal reorganization. Additionally, these cells can be employed in Wnt reporter assays, RNA-seq profiling of downstream targets, apoptosis analyses, and drug sensitivity screens to evaluate therapeutic vulnerabilities. For further information or to request a quote, please contact Ascent Research.
