The ITGA6 Knouckout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 cells with targeted disruption of the ITGA6 gene. This polyclonal knockout product provides a heterogeneous loss-of-function model, avoiding clonal artifacts of single-cell-derived lines. The knockout status should be validated by end users via Western blotting or immunofluorescence to confirm reduced integrin alpha-6 expression.
SK-HEP-1 is a human hepatic adenocarcinoma cell line originally isolated from ascites of a patient with liver adenocarcinoma. Though classified as liver cancer, it displays a gene expression signature resembling liver sinusoidal endothelial cells (LSECs), making it a useful model for tumor microenvironment studies. The adherent, epithelial-like cells are widely employed in cancer research, notably for investigating hepatocellular carcinoma metastasis and angiogenesis.
ITGA6 encodes integrin alpha-6, which dimerizes with beta-1 or beta-4 to form laminin-binding receptors. Laminin engagement activates focal adhesion kinase (FAK) and Src, driving PI3K/AKT and MAPK/ERK pathways that promote survival, proliferation, and migration. Key downstream effectors include Rho GTPases (RhoA, Rac1, Cdc42) and matrix metalloproteinases. Upstream regulators comprise growth factors (EGF, HGF), cytokines (TGF-beta), and transcription factors (MYC, TP53). ITGA6 knockout abrogates laminin-mediated adhesion and disrupts these signaling cascades.
Given SK-HEP-1??s hepatic and endothelial features, ITGA6 knockout is pertinent for studying laminin-dependent processes in liver cancer. Loss of ITGA6 is expected to impair attachment to laminin-rich substrates, reduce FAK/Src signaling, and attenuate migratory and invasive capabilities. This model facilitates exploration of integrin alpha-6 in tumor-stroma crosstalk, transendothelial migration, and vascular mimicry.
Applications include quantitative laminin adhesion assays, transwell migration and Matrigel invasion assays, phospho-signaling profiling by Western blotting for FAK, AKT, and ERK, flow cytometry to confirm integrin alpha-6 loss, and co-culture systems with liver stromal cells. The cells also support drug screening for integrin-targeted therapies and transcriptomic studies via RNA-seq. For further details, contact Ascent Research.
