The ABI1 Knockout Huh-7 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of Huh-7 hepatocellular carcinoma cells with targeted disruption of the ABI1 gene. This polyclonal model provides a heterogeneous loss-of-function system for studying ABI1-dependent processes without clonal isolation. It enables bulk analysis of migration, signaling, and cytoskeletal dynamics in a liver cancer context.
The Huh-7 host cell line is a well-differentiated hepatocellular carcinoma derived from a 57-year-old Japanese male liver tumor. Widely used as an HCC model, Huh-7 cells exhibit epithelial morphology and key hepatic functions. Their tumorigenic and migratory properties make them suitable for investigating cancer metastasis and therapeutic responses.
ABI1 is an adaptor protein linking Abl kinases (ABL1, ABL2) to the WAVE regulatory complex, promoting Arp2/3-mediated actin polymerization and lamellipodia formation. It is activated downstream of receptor tyrosine kinases (PDGFR, EGFR) and adhesion signals, and interacts with WAVE components (CYFIP1, NCKAP1, WASF2) as well as EPS8 and SOS1. ABI1 thereby regulates cell migration, adhesion, and immune synapse organization.
In Huh-7 cells, ABI1 disruption impairs lamellipodia assembly, reducing directional migration and invasion??key processes in HCC metastasis. This knockout model allows dissection of ABI1’s role in tumor cell motility, epithelial-mesenchymal transition, and response to chemotactic cues. It also aids in evaluating Abl kinase-targeted therapies and resistance mechanisms.
Applications include wound healing and Transwell migration/invasion assays, immunofluorescence for actin cytoskeleton, Western blotting for ABI1 and phospho-Abl, RT-qPCR, and co-immunoprecipitation. The polyclonal cells support drug response profiling and high-content screening. Ascent Research offers expert support for assay optimization and data analysis.
