The ITGB6 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of SK-HEP-1 hepatic epithelial cells, generated by ITGB6 gene disruption for loss-of-function studies. This heterogeneous pool enables investigation of integrin ??6-dependent biology in bulk assays and phenotypic screens without clonal selection.
SK-HEP-1 is a human liver adenocarcinoma cell line with epithelial morphology, widely used as a model for hepatocellular carcinoma and hepatic fibrosis. These cells exhibit TGF-?? responsiveness and key features of epithelial-mesenchymal transition (EMT), providing a relevant context for ITGB6 function in tumor microenvironment and fibrogenesis.
ITGB6 encodes the integrin ??6 subunit, which heterodimerizes with ??V to form the ??V??6 receptor. This integrin binds RGD ligands, notably LAP-TGF-??, to activate latent TGF-??. ITGB6 expression is regulated by TGF-??, TNF-??, EGF, and AP-1, creating feedback amplification. Downstream, ??V??6 activates SMAD2/3 signaling, leading to transcriptional induction of PAI-1, collagen, and CTGF, with parallel non-canonical ERK/AKT pathways. Key interacting partners include fibronectin, talin, kindlin, FAK, and Src. Disruption of ITGB6 eliminates ??V??6-mediated TGF-?? activation and associated signaling.
In the SK-HEP-1 liver cancer background, ITGB6 knockout provides a model to dissect ??V??6 integrin roles in tumor progression and fibrosis. Loss of ITGB6 is expected to impair SMAD2/3 and ERK/AKT signaling, reducing adhesion, migration, and fibrotic marker expression. This model allows isolation of integrin-specific TGF-?? activation and supports anti-fibrotic drug screening.
The polyclonal knockout cells are suitable for Western blot (ITGB6, phospho-SMAD2), RT-qPCR (PAI-1, CTGF), adhesion assays on fibronectin, TGF-?? bioassays, migration/invasion studies, immunofluorescence, and flow cytometry. These applications facilitate research on integrin function, TGF-?? activation, liver cancer progression, and fibrosis therapies. For further details, contact Ascent Research.
