The ABLIM3 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-mediated polyclonal knockout population of the human hepatocellular carcinoma cell line SK-HEP-1, in which the ABLIM3 gene has been disrupted. This polyclonal pool results from non-clonal expansion after gene editing, offering a heterogeneous cellular mixture that reflects the complexity of a knockout model without single-cell cloning. The targeted disruption of ABLIM3 enables loss-of-function studies in a liver cancer context, facilitating the investigation of actin cytoskeletal dynamics and cell adhesion pathways.
SK-HEP-1 is a widely used hepatocellular carcinoma cell line originally derived from the ascitic fluid of a patient with liver adenocarcinoma. This adherent epithelial line exhibits characteristics of malignant hepatocytes and is extensively employed in cancer research, particularly for studies on tumor cell migration, invasion, and metastasis. Its genetic background, including TP53 and beta-catenin mutations, makes it a relevant model for hepatic carcinogenesis and the evaluation of genes implicated in hepatocellular carcinoma progression.
ABLIM3 encodes an actin-binding LIM domain protein that functions as a scaffolding molecule, organizing the actin cytoskeleton and regulating focal adhesion dynamics. It integrates signals from upstream regulators such as integrin-mediated adhesion, TGF-beta, and focal adhesion kinase (FAK), and modulates downstream effectors including cofilin, RhoA, and Rac1. Through direct interactions with filamentous actin, vinculin, paxillin, and the Hippo pathway kinase LATS1, ABLIM3 bridges actin filaments to focal adhesion complexes, influencing cytoskeletal tension, lamellipodia formation, and cell motility. ABLIM3 also intersects with Wnt signaling, adding another layer of control to cellular behavior.
In the context of hepatocellular carcinoma, ABLIM3 is thought to exert tumor-suppressive functions by maintaining stable cell?Cmatrix adhesions and restricting migratory and invasive capacities. Knockout of ABLIM3 in SK-HEP-1 cells is expected to perturb actin reorganization and focal adhesion turnover, potentially enhancing metastatic phenotypes. This model therefore provides a pertinent system to dissect the molecular underpinnings of HCC cell dissemination, evaluate the crosstalk between actin dynamics and oncogenic signaling, and explore ABLIM3??s role in suppressing epithelial?Cmesenchymal transition.
This polyclonal knockout product supports a broad range of experimental approaches. Researchers can utilize western blotting and RT-qPCR to confirm ABLIM3 ablation and study transcriptional changes, immunofluorescence to visualize actin stress fibers and focal adhesions, and co-immunoprecipitation to analyze protein interactions with vinculin, paxillin, or LATS1. Functional assays, including wound healing and transwell invasion experiments, can quantify cell migration and invasion, while apoptosis assays may reveal links to cell survival. The model is particularly suited for investigating how ABLIM3 loss modulates responses to TGF-beta treatment or integrin-dependent signaling. For further information and technical support, please contact Ascent Research.
