DST Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the DST gene in Huh-7 hepatocellular carcinoma cells. This polyclonal format provides a genetically diverse pool with stable dystonin loss, avoiding clonal selection artifacts. The CRISPR/Cas9-mediated gene disruption creates a reliable loss-of-function model for studying DST-dependent processes. Suitable for population-level analyses, this product enables robust functional investigations without clone-specific biases.
The Huh-7 cell line, derived from a human hepatocellular carcinoma of a Japanese male, exhibits epithelial morphology and hepatocyte-like characteristics. Widely used in liver cancer research, these cells retain liver-specific functions and are suited for adhesion, migration, and cytoskeletal studies. Their well-characterized genetic background, including p53 mutations, provides a clinically relevant platform for tumor biology and metastasis assays.
DST encodes dystonin, a plakin family cytolinker connecting intermediate filaments to actin and microtubules. It interacts with actin, tubulin, and ??4 integrin, and is regulated by integrins, mechanical stress, and TGF-??. Dystonin functions downstream of FAK and paxillin to promote actin polymerization and focal adhesion turnover. Via the integrin ??1?Ctalin?Cvinculin axis, it mediates mechanotransduction. DST disruption uncouples the cytoskeleton from the matrix, impairing adhesion and signaling.
In Huh-7 liver cancer cells, DST loss compromises cell adhesion, migration, and invasiveness due to defective integrin?Ccytoskeleton linkage. This model mimics aspects of tumor cell dissemination and anoikis resistance, relevant to hepatocellular carcinoma metastasis. It allows dissection of how cytoskeletal disorganization influences integrin signaling and uncovers compensatory mechanisms. The polyclonal knockout pool is valuable for identifying vulnerabilities in cancer cells reliant on mechanically coupled adhesion.
Applications include cell adhesion, scratch wound migration, and transwell invasion assays to quantify motility defects. Western blotting and immunofluorescence confirm dystonin loss and cytoskeletal changes. Drug sensitivity assays screen for integrin pathway inhibitors or adhesion-targeted compounds. The model also supports research on hereditary sensory and autonomic neuropathy type 6 and epidermolysis bullosa in a hepatic context. For detailed information, contact Ascent Research.
