The EHBP1L1 Knockout Huh-7 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population derived from Huh-7 hepatocellular carcinoma cells, with targeted disruption of the EHBP1L1 gene. This loss-of-function model is generated to enable functional studies of EHBP1L1 in a relevant hepatic tumor context without introducing monoclonal selection or clonal artifacts. The polyclonal format captures the heterogeneity of genomic edits within the population, facilitating robust downstream analyses while maintaining a wild-type genetic background for the non-targeted loci.
Huh-7 cells are a widely used human hepatocellular carcinoma line originally isolated from a liver tumor of a 57-year-old Japanese male. They retain epithelial morphology and are permissive to hepatitis C virus replication, making them a standard model for liver cancer biology, viral host interactions, and drug screening. The parental cell line exhibits active actin dynamics and Rab-dependent trafficking pathways, providing a physiologically relevant platform to investigate EHBP1L1 function in hepatocarcinogenesis and metastatic progression.
EHBP1L1 (EH domain-binding protein 1-like 1) encodes a scaffold protein that bridges Rab8 GTPase signaling to the actin cytoskeleton. It functions downstream of active, GTP-bound Rab8 and simultaneously interacts with actin filaments and the adaptor protein EHBP1. Through these interactions, EHBP1L1 coordinates Rab8-mediated vesicle trafficking with actin remodeling, thereby regulating endocytic recycling and cell migration. The protein is also associated with focal adhesion complexes, linking membrane trafficking to dynamic control of cell?Cmatrix adhesion.
In Huh-7 hepatocellular carcinoma cells, EHBP1L1 is implicated in the modulation of migratory and invasive phenotypes. Disruption of EHBP1L1 is anticipated to impair Rab8-dependent trafficking events required for directed cell movement, leading to reduced actin cytoskeletal reorganization and diminished focal adhesion turnover. Consequently, this polyclonal knockout model serves as a powerful tool for dissecting the molecular mechanisms underlying liver cancer cell motility, extravasation, and metastatic colonization, and for evaluating the dependency of tumor cell migration on EHBP1L1-Rab8-actin axis integrity.
Researchers can employ this knockout cell product in a wide array of functional assays, including wound healing and Transwell invasion assays to measure migration and invasion, immunofluorescence staining of actin filaments to visualize cytoskeletal changes, and western blotting to confirm loss of EHBP1L1 protein. Co-immunoprecipitation experiments can further probe the disruption of the EHBP1L1?CRab8 interaction, while cell adhesion assays assess alterations in substrate attachment. This polyclonal knockout model serves as a versatile tool for dissecting EHBP1L1-dependent mechanisms and for screening anti-metastatic compounds in hepatocellular carcinoma. For additional product details or technical inquiries, please contact Ascent Research.
