The ITGA1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout pool derived from the human hepatic adenocarcinoma cell line SK-HEP-1. This cellular model features targeted disruption of the ITGA1 gene, which encodes the integrin alpha-1 subunit, a key mediator of cell-extracellular matrix interactions. The polyclonal format comprises a mixed population of cells bearing Cas9-induced mutations at the ITGA1 locus, enabling robust functional analyses without clonal bias.
SK-HEP-1 is a well-characterized liver adenocarcinoma line isolated from the ascites of a patient with liver adenocarcinoma. It exhibits a mesenchymal, invasive phenotype, making it relevant for studies of hepatocellular carcinoma metastasis and epithelial-mesenchymal transition. These cells attach and migrate on collagen and laminin in an alpha1beta1 integrin-dependent manner, providing a disease-relevant system to examine ITGA1 function.
ITGA1 pairs with ITGB1 to form the alpha1beta1 heterodimer, which serves as a primary receptor for collagens and laminins. Ligand engagement triggers focal adhesion kinase (FAK; PTK2) phosphorylation at Tyr397, initiating signaling cascades involving SRC, AKT1, and MAPK1 (ERK2). Signaling is modulated by upstream regulators TGFB1, TNF, IL1B, and EGF, and the receptor complex is anchored by talin and vinculin. Disruption of ITGA1 abolishes heterodimer formation, blocking FAK activation and reducing phosphorylation of downstream effectors PXN, RAC1, and RHOA, consequently impairing adhesion, migration, and proliferation.
In the SK-HEP-1 context, ITGA1 knockout allows dissection of alpha1beta1 integrin contributions to liver cancer progression. ITGA1 has been linked to hepatocellular carcinoma metastasis, liver fibrosis, and inflammatory signaling. This polyclonal knockout pool facilitates systematic study of how loss of collagen/laminin adhesion impacts tumor cell behavior and crosstalk between integrin and growth factor-driven pathways, including PI3K-Akt and MAPK cascades.
Applications include transwell migration/invasion assays, cell adhesion assays on collagen or laminin substrates, immunofluorescence staining of focal adhesion proteins, and phospho-FAK detection by western blotting. Flow cytometry can verify surface integrin alpha-1 loss, and RT-qPCR can profile transcriptional changes. This versatile model supports cancer cell adhesion and invasion research, ECM interaction studies, and drug target validation. For further details or technical support, contact Ascent Research.
