The DPYSL2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This heterogeneous pool of gene-disrupted cells enables loss-of-function studies of DPYSL2 (encoding collapsin response mediator protein 2, CRMP2) without the need for single-cell cloning. The polyclonal format offers a rapid, cost-effective approach to assess DPYSL2 function in a liver cancer background, reflecting the collective knockout effects across a diverse cell population. By preserving natural cellular variation, this product is particularly suited for high-throughput screening and assays that demand robust, population-level phenotypes.
SK-HEP-1 cells were originally isolated from the ascites of a 56-year-old male with liver adenocarcinoma and are widely used as a model for hepatic adenocarcinoma. These adherent cells display a mixed phenotype combining features of hepatocellular carcinoma and endothelial-like cells, making them valuable for studies of tumor-endothelial interactions and metastasis. The cell line grows robustly in standard culture conditions and demonstrates high invasive potential, facilitating investigations into cancer cell migration and invasion. The SK-HEP-1 background provides a relevant disease context for evaluating the role of DPYSL2 in liver cancer pathology.
DPYSL2 encodes CRMP2, a phosphoprotein that regulates cytoskeletal dynamics via interactions with microtubules and actin. CRMP2 functions downstream of semaphorin-3A through the neuropilin-1/plexin-A1 receptor complex, with its activity modulated by GSK-3?? phosphorylation. It directly binds ??-tubulin, ??-tubulin, and kinesin-1, and associates with CRMP family members (CRMP1, CRMP3, CRMP4). CRMP2 governs axon guidance and cell migration by controlling actin reorganization through cofilin phosphorylation and RhoA/ROCK signaling, as well as microtubule assembly, thus linking semaphorin and integrin pathways to cytoskeletal remodeling, focal adhesion turnover, and cell motility.
In the hepatic adenocarcinoma context, DPYSL2 knockout disrupts the cytoskeletal remodeling essential for cancer cell migration and invasion, which are critical steps in metastasis. Given that SK-HEP-1 cells are highly invasive, loss of CRMP2 function is expected to impair semaphorin-3A-mediated repulsive signaling and downstream actin dynamics, reducing the cells’ ability to traverse extracellular matrix barriers. This model thus provides a direct tool to assess the role of CRMP2 in liver cancer progression and to identify signaling dependencies within the Rho GTPase and MAPK/ERK pathways that govern invasive behavior.
Researchers can employ this polyclonal knockout model in diverse applications including tumor invasion and metastasis studies, cytoskeleton dynamics research, and semaphorin signaling pathway analysis. Representative assays include Western blotting and RT-qPCR to confirm DPYSL2 disruption, scratch wound healing and Transwell migration/invasion assays to evaluate cell motility, and immunofluorescence for F-actin and ??-tubulin to visualize cytoskeletal organization. Additional biochemical approaches such as co-immunoprecipitation with ??-tubulin and RhoA activity assays can probe protein complexes and signaling activities. For further technical information, please contact Ascent Research.
