The DST Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population specifically designed to disrupt the DST gene (encoding dystonin/BPAG1) in the SK-HEP-1 human liver adenocarcinoma cell line. This loss-of-function model enables researchers to investigate the functional consequences of abolishing this critical cytoskeletal linker protein in a tumorigenic epithelial context. The polyclonal nature of the product reflects a mixed population of edited cells, providing a robust system for studying DST-dependent phenotypes without the confounding effects of single-cell clonal selection.
The parental SK-HEP-1 cell line is a well-established human liver adenocarcinoma epithelial model derived from the ascitic fluid of a patient with hepatic adenocarcinoma. These cells exhibit tumorigenic properties and are widely employed to study hepatocellular carcinoma progression, metastasis, and epithelial?Cmesenchymal transition. Their aggressive phenotype and retention of key hepatocyte-like features make them particularly suitable for investigating the cytoskeletal dynamics that underlie invasive migration and metastatic dissemination.
DST encodes a large plakin family cytoskeletal linker protein that physically connects intermediate filaments (such as keratins) to actin microfilaments and microtubules, thereby maintaining cellular mechanical integrity, focal adhesions, and directed migration. In the signaling network, DST functions downstream of TP63 and integrin-mediated adhesion, and is regulated by TGF-?? signaling. It stabilizes keratin filament networks and organizes the actin cytoskeleton through interactions with F-actin, keratin 8/18, plectin, BP180, integrin ??6??4, and ERM proteins. Disruption of DST leads to impaired focal adhesion dynamics, compromised Rho GTPase signaling, and altered mechanotransduction, highlighting its central role in coordinating cytoskeletal architecture.
In SK-HEP-1 cells, which rely on dynamic cytoskeletal remodeling for invasion and metastasis, DST knockout profoundly disrupts intermediate filament organization and focal adhesion stability. The resulting loss of cell?Cmatrix adhesion and attenuated migratory capacity are expected to reduce the invasive potential of these adenocarcinoma cells. This model thus illuminates the mechanistic contributions of the DST scaffold to hepatic tumor progression, particularly in the context of cancer cell dissemination and colonization of distant sites.
This knockout cell model is ideally suited for a broad range of functional studies. Researchers can employ Transwell migration and invasion assays to quantify metastatic behavior, immunofluorescence microscopy to visualize keratin and actin cytoskeleton disorganization, and Western blotting to assess focal adhesion components such as FAK and paxillin. Additional recommended assays include cell adhesion assays on extracellular matrix substrates, Rho GTPase activation assays (e.g., G-LISA) to probe downstream signaling, and RNA-seq transcriptome profiling to capture global expression changes. These applications support investigations into anti-metastatic drug screening, plakin family gene knockout phenotyping, and the molecular dissection of hemidesmosome component functions. For further details, pricing, and ordering information, please contact Ascent Research.
