The DOCK7 Knockout Huh-7 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population designed for DOCK7 gene disruption in the Huh-7 hepatocellular carcinoma background. This robust loss-of-function model is ideal for investigating DOCK7-mediated cytoskeletal dynamics and cell migration. The polyclonal format ensures a heterogeneous allelic mixture, providing biological relevance for functional studies, including those requiring population-level response assessments. Researchers can utilize this tool in diverse assays, from biochemical signaling analyses to phenotypic migration assessments.
The host cell line, Huh-7, is an epithelial adherent cell line derived from hepatocellular carcinoma of a 57-year-old Japanese male. Retaining key hepatocyte features, these cells are extensively used in liver cancer and hepatitis C virus (HCV) studies. The well-characterized nature and genetic tractability of Huh-7 cells make them an excellent platform for creating knockout models to dissect pathways in hepatocarcinogenesis. The extensive background data aids interpretation of results from the DOCK7-deficient derivative.
DOCK7 is a dual-function protein acting as a guanine nucleotide exchange factor (GEF) for the small GTPases Rac1 and Cdc42, and localizing to centrosomes via TACC3 to phosphorylate the microtubule-destabilizing protein stathmin (STMN1). Its GEF activity activates downstream PAK1/2 and the WAVE complex, driving actin polymerization and lamellipodia formation. Simultaneously, DOCK7-mediated phosphorylation of stathmin modulates microtubule dynamics, essential for cell polarity and directed migration. Thus, DOCK7 coordinates actin and microtubule networks, integrating inputs from Rho GTPase pathways and centrosomal signals.
In the Huh-7 context, DOCK7 disruption is particularly pertinent for modeling metastatic behavior and cytoskeletal dysregulation. Eliminating DOCK7 allows dissection of Rac1- and Cdc42-dependent signaling cascades governing motility, invasion, and microtubule stability. Researchers can assess how loss of DOCK7 alters PAK activation and stathmin phosphorylation, offering mechanistic insight into liver cancer aggressiveness. The model also enables evaluation of compensatory responses within the Rho GTPase network upon DOCK7 ablation, deepening understanding of signaling plasticity.
This product supports a variety of applications, including scratch wound migration assays, transwell invasion studies, G-LISA activation tests for Rac1 and Cdc42, and immunofluorescence visualization of actin filaments and microtubules. It serves as a valuable tool for functional genomics, enabling elucidation of DOCK7-dependent signaling in hepatoma cells. Additionally, the cells can be used in drug screening to identify compounds targeting Rho GTPase pathways or microtubule dynamics for anti-metastatic development. For further information, please contact Ascent Research.
