The L1CAM Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate L1CAM expression in the SK-HEP-1 human hepatocellular carcinoma line. This product consists of a heterogeneous pool of cells harboring targeted gene disruption, allowing the study of L1CAM loss-of-function effects without the clonal variability associated with single-cell-derived lines. The polyclonal format provides a robust model system for examining L1CAM-dependent phenotypes in a population-averaged context, suitable for high-throughput screening and functional genomics applications.
SK-HEP-1 is a well-characterized human liver adenocarcinoma cell line established from the ascites of a patient with hepatocellular carcinoma. These cells exhibit an epithelial morphology and are widely utilized in cancer research to investigate hepatocarcinogenesis, metastasis, and drug resistance mechanisms. The SK-HEP-1 line retains key features of liver cancer cells, including active integrin signaling and a constitutively activated MAPK/ERK pathway, thereby providing a relevant cellular context for dissecting the role of cell adhesion molecules in tumor progression.
L1CAM (L1 cell adhesion molecule) is a type I transmembrane glycoprotein that mediates cell adhesion, migration, and invasion via homophilic binding and heterophilic interactions with integrins (??v??3, ??5??1) and FGFR1. These interactions activate FAK and Src kinases, leading to ERK1/2 and AKT phosphorylation, and drive NF-??B-dependent transcription of pro-invasive genes such as MMP2 and MMP9. Upstream, the Wnt/??-catenin pathway and TGF-??1 signaling regulate L1CAM expression through the transcription factors SLUG and the ??-catenin/TCF complex. Consequently, L1CAM orchestrates a signaling network that integrates extracellular matrix cues with intracellular effector pathways to promote cancer cell dissemination.
In SK-HEP-1 hepatocellular carcinoma cells, L1CAM is frequently overexpressed and correlates with a mesenchymal, invasive phenotype and resistance to chemotherapeutic agents. The knockout of L1CAM in this cell model is expected to impair integrin-dependent adhesion, decrease FAK and ERK1/2 phosphorylation, and reduce the activity of MMP2/9, leading to diminished migration and invasion capacities. Furthermore, loss of L1CAM may sensitize cells to apoptosis by attenuating AKT-mediated survival signals, making this a valuable tool for studying the molecular basis of chemoresistance in liver cancer.
This polyclonal L1CAM knockout cell pool enables diverse research applications, including migration and invasion assays, drug sensitivity profiling, and phospho-signaling analyses using techniques such as Western blotting for phospho-ERK or phospho-FAK, RT-qPCR for downstream effectors, and immunofluorescence for adhesion structures. The model is particularly valuable for studying L1CAM??s role in metastasis and chemoresistance in hepatocellular carcinoma, and may also inform neurodevelopmental disorder mechanisms. For further inquiries, please contact Ascent Research.
