The DOCK7 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma line. This mixed population harbors targeted disruptions within the DOCK7 gene, generating a functional loss-of-function model suitable for studying DOCK7-dependent pathways in a cancerous epithelial background. The polyclonal format ensures a diverse representation of editing events while maintaining robust target-gene silencing across the population, enabling flexible experimental designs without clonal selection bias.
The parental SK-HEP-1 cell line was originally isolated from the ascitic fluid of a male patient with liver adenocarcinoma. These adherent epithelial cells exhibit characteristic features of metastatic cancer cells, including high migratory and invasive capacity, making them an established model for liver cancer biology and metastasis research. Their tumorigenic origin provides a physiologically relevant context for investigating the role of cytoskeletal and adhesion regulators in cancer progression.
DOCK7 functions as a guanine nucleotide exchange factor for the small GTPases Rac1 and Cdc42, acting as a critical upstream activator of actin cytoskeleton reorganization, cell migration, and adhesion. DOCK7 is recruited and activated through PI3K/PIP3 and integrin signaling, often in association with ELMO1 and ELMO2 scaffold proteins. Once activated, DOCK7 promotes GTP loading on Rac1 and Cdc42, which in turn trigger effector kinases such as PAK1 and the WAVE2?CArp2/3 complex to drive actin polymerization and lamellipodia formation. Additionally, DOCK7 interacts with microtubules, linking actin and microtubule cytoskeletal dynamics.
Disruption of DOCK7 in SK-HEP-1 cells abrogates Rac1/Cdc42-mediated cytoskeletal regulation, leading to impaired cell migration, defective adhesion, and altered actin architecture. Given the inherent metastatic potential of SK-HEP-1 cells, this knockout model is particularly valuable for dissecting the molecular mechanisms underlying cancer cell dissemination and invasion. Moreover, as DOCK7 mutations are associated with neurodevelopmental disorders, including early infantile epileptic encephalopathy and intellectual disability, the SK-HEP-1 background offers a complementary system to probe DOCK7-dependent neuronal migration and adhesion pathways in a tractable in vitro setting.
This polyclonal knockout cell product supports a wide range of experimental approaches. Typical applications include quantitative cell migration assays such as wound healing and transwell migration, immunofluorescence staining to visualize actin cytoskeletal reorganization, biochemical pull-downs to assess Rac1 and Cdc42 activation status, western blotting for downstream effectors (e.g., PAK1, WAVE2), and cell adhesion assays. These tools are instrumental for studies in cancer metastasis, neurodevelopmental disease modeling, and cytoskeletal pharmacology. For additional information or custom inquiries, please contact Ascent Research.
