The ITIH2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1. This product provides a heterogeneous pool of ITIH2-disrupted cells, generated by CRISPR/Cas9-mediated gene disruption, offering a robust loss-of-function model for functional studies. The polyclonal format minimizes clonal bias and represents a population-level knockout effect, suitable for diverse experimental applications.
SK-HEP-1 is a well-characterized human hepatic adenocarcinoma cell line exhibiting both endothelial and epithelial features, commonly employed as a model for liver sinusoidal endothelial cells or hepatocellular carcinoma (HCC) research. Its dual phenotype enables investigations into hepatic tumor biology, extracellular matrix interactions, and endothelial functions such as hyaluronan metabolism and cell migration.
ITIH2 encodes the heavy chain H2 of inter-alpha-trypsin inhibitor (ITI), a serine protease inhibitor that stabilizes the extracellular matrix by covalently linking to hyaluronan. This process is mediated by TSG-6 and involves complex formation with bikunin (AMBP) and other heavy chains (ITIH1, ITIH3, ITIH4). ITIH2 is regulated by pro-inflammatory cytokines (IL-6, TNF-alpha), TGF-beta, and NF-kB signaling, and functions to inhibit serine proteases like trypsin, plasmin, and neutrophil elastase. The ITIH2-hyaluronan interaction is critical for pericellular matrix formation and influences cell migration and proliferation downstream.
In SK-HEP-1 cells, ITIH2 knockout is anticipated to impair hyaluronan stabilization and extracellular matrix remodeling, impacting cell adhesion, migration, and invasion. This model enables dissection of HCC metastasis mechanisms and liver sinusoidal endothelial biology, particularly how ITIH2-mediated matrix stability modulates inflammation and protease inhibition within the hepatic microenvironment.
Applications include studying extracellular matrix dynamics, HCC metastasis, hyaluronan-mediated signaling, inflammation, tumor microenvironment, and liver fibrosis. Assays such as Western blotting, RT-qPCR, hyaluronan binding, cell migration/invasion, co-immunoprecipitation, protease activity, and immunofluorescence are compatible. This knockout model supports drug discovery and mechanistic investigations of ITIH2-dependent pathways. For further details, please contact Ascent Research.
