The DOCK11 Knockout Huh-7 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of Huh-7 hepatocellular carcinoma cells with targeted disruption of the DOCK11 gene. This heterogeneous knockout pool enables investigation of DOCK11 function without clonal selection artifacts, providing a robust model for studying gene-dependent phenotypes in cell migration, adhesion, and signaling. It is directly applicable to assays probing actin cytoskeletal dynamics and CDC42-related pathways in a liver cancer context.
Huh-7 cells are a well-differentiated human hepatocellular carcinoma line expressing alpha-fetoprotein and albumin, with multiple chromosomal aberrations. As a hepatic epithelial model, Huh-7 is widely used for studying hepatocellular carcinoma progression, including cell motility and invasion. Its tumorigenic properties and retention of hepatocyte features make it a relevant host for investigating oncogenic signaling networks.
DOCK11 is a guanine nucleotide exchange factor for CDC42, activated by upstream signals including PIP3 and receptor tyrosine kinases (e.g., EGFR, PDGFR) via SRC family kinases. It catalyzes GTP loading onto CDC42, triggering downstream effectors PAK1/2 and WASL/WASP, which regulate LIMK/cofilin-mediated actin dynamics and filopodia formation. DOCK11 also interacts with ELMO1/2 and Nck to couple integrin signaling to cytoskeletal reorganization. Thus, DOCK11 links PI3K?CPIP3 signaling to CDC42-driven cell migration and adhesion.
In Huh-7 cells, DOCK11-dependent CDC42 activation promotes migration and invasion, contributing to hepatocellular carcinoma metastatic potential. Disrupting DOCK11 in this model allows direct analysis of how DOCK11 modulates actin-based motility and tumor cell behavior. This knockout tool facilitates studies aimed at clarifying the role of DOCK11 in liver cancer progression and evaluating intervention strategies targeting the DOCK11?CCDC42 axis.
This polyclonal knockout line is suitable for wound healing and Transwell migration/invasion assays, coupled with immunofluorescence for F-actin and focal adhesions. Western blotting for phospho-PAK1 and cofilin, co-immunoprecipitation of DOCK11 complexes, and live-cell imaging of actin dynamics provide mechanistic insights. Researchers can also employ the model for anti-metastatic drug testing and phospho-signaling array analyses. For further information, please contact Ascent Research.
