CCDC25 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 human hepatocellular carcinoma cell line. This product provides a loss-of-function model for the CCDC25 gene, offering a heterogeneous pool of edited cells suitable for bulk functional studies. The polyclonal format preserves genetic complexity while enabling efficient disruption of the target gene across the population.
The Huh-7 cell line is a well-differentiated human hepatocellular carcinoma model established from a liver tumor. It maintains epithelial morphology and is widely employed in studies of hepatocarcinogenesis, hepatitis C virus replication, and liver cancer biology. This cell line expresses typical hepatocyte markers and exhibits robust growth characteristics, making it a reliable platform for gene-editing studies.
CCDC25 functions as a cell surface receptor for DNA released from neutrophil extracellular traps (NETs). Upon binding extracellular NET-DNA, CCDC25 activates the integrin-linked kinase (ILK) and its adaptor beta-parvin, which in turn signal to the small GTPases RAC1 and CDC42. This cascade promotes actin cytoskeleton polymerization and remodeling, enhancing cell motility and invasive capacity. Consequently, CCDC25 serves as a molecular link between the tumor microenvironment and metastatic progression, particularly in hepatocellular carcinoma.
In the context of Huh-7 cells, which are derived from liver cancer, disruption of CCDC25 provides a physiologically relevant model to dissect the NET-DNA signaling axis and its contribution to hepatocellular carcinoma metastasis. The knockout allows researchers to assess the dependence of migratory and invasive phenotypes on CCDC25, delineate downstream signaling events, and evaluate the impact on actin dynamics.
These cells are suitable for a wide range of experimental approaches. Researchers can validate CCDC25 knockout by Western blotting or RT-qPCR, perform Transwell migration and invasion assays to quantify motility changes, visualize actin cytoskeleton reorganization by immunofluorescence, and probe protein?Cprotein interactions such as those between CCDC25 and ILK through co-immunoprecipitation. The polyclonal knockout population also serves as a tool for high-content screening of compounds that may inhibit the CCDC25-dependent metastatic pathway. For further technical details or inquiries, please contact Ascent Research.
