The ARPC5L Knockout SK-HEP-1 Polyclonal Cells are a polyclonal cell population derived from the SK-HEP-1 human liver adenocarcinoma line, engineered by CRISPR/Cas9-mediated disruption of the ARPC5L gene. This heterogeneous knockout model enables functional studies of ARPC5L in a hepatocellular carcinoma context, providing a mixed population of edited cells without clonal selection artifacts.
The parental SK-HEP-1 cell line, isolated from the ascites of a liver adenocarcinoma patient, is an adherent model of hepatocellular carcinoma with inherent metastatic and invasive properties. It is widely used to study mechanisms of liver cancer progression, cell migration, and cytoskeletal reorganization.
ARPC5L encodes a subunit of the Arp2/3 complex that nucleates actin filament branching. ARPC5L is activated downstream of Rac1 and CDC42 GTPases through the WAVE regulatory complex and cortactin, and it mediates lamellipodia formation, focal adhesion turnover, and directional cell migration. It interacts directly with other Arp2/3 subunits (ARPC1A, ARPC1B, ARPC2, ARPC3, ARPC4) and actin, and is regulated by upstream factors including PIP2, PI3K, and WASP/N-WASP family proteins.
In SK-HEP-1 cells, ARPC5L knockout disrupts branched actin networks, impairing lamellipodial protrusion and migration, thereby attenuating metastatic behavior. This loss-of-function model is valuable for dissecting how actin dynamics drive liver cancer metastasis and for evaluating cytoskeletal-targeted therapies.
Applications include mechanistic studies of Arp2/3 complex function, anti-metastatic drug screening, and in vitro modeling of liver cancer progression. Compatible assays encompass Western blotting for ARPC5L, immunofluorescence staining of F-actin, wound healing, Transwell migration and invasion assays, live-cell imaging of actin dynamics, co-immunoprecipitation of the Arp2/3 complex, and Rac1-GTP phospho-signaling analysis. For detailed technical specifications or custom cell engineering requests, please contact Ascent Research.
