The DNMBP Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 hepatocellular carcinoma cell line, designed for loss-of-function studies of the DNMBP gene. This product provides a genetically heterogeneous pool of cells harboring targeted disruptions of the DNMBP locus, enabling researchers to investigate gene function without clonal selection artifacts. The polyclonal format preserves cellular diversity while achieving effective knockout of DNMBP expression, making it suitable for population-level analyses of signaling, migration, and cytoskeletal dynamics.
The Huh-7 cell line is a well-characterized human hepatocellular carcinoma model isolated from a 57-year-old Japanese male. It is extensively used in liver cancer biology, hepatitis C virus replication, and hepatic metabolism research, offering a tumorigenic context with retained hepatocyte functions. Huh-7 cells serve as an appropriate host for examining oncogenic pathways relevant to hepatocarcinogenesis and metastatic progression.
DNMBP encodes a scaffold protein and Cdc42 guanine nucleotide exchange factor that orchestrates actin cytoskeleton remodeling, membrane trafficking, and cell junction assembly by linking dynamin with actin regulatory proteins. It is activated downstream of receptor tyrosine kinases such as EGFR, integrin signaling, and Src family kinases, and promotes Cdc42-mediated activation of N-WASP and the Arp2/3 complex, leading to actin polymerization and filopodia formation. DNMBP also interacts with cortactin, WIP, and actin, and modulates tight junction dynamics through the Cdc42-PAK1-LIMK-cofilin pathway, underscoring its central role in coordinating cytoskeletal and junctional organization.
In the Huh-7 hepatocellular carcinoma context, DNMBP knockout disrupts Cdc42-dependent cytoskeletal remodeling, impairing cell migration, invasion, and tight junction integrity. This model is instrumental for dissecting molecular mechanisms driving hepatocellular carcinoma progression, metastasis, and epithelial-to-mesenchymal transition. It may also be applied to study the role of DNMBP polymorphisms in celiac disease susceptibility within an epithelial tumor background, offering insights into disease-associated variants.
This polyclonal knockout cell population is optimized for functional assays including Transwell migration and invasion, wound healing, and phalloidin staining to assess F-actin reorganization. Researchers can further utilize Cdc42 activity pull-downs, immunofluorescence for tight junction markers such as ZO-1 and occludin, western blotting of actin regulatory proteins, and RT-qPCR for EMT markers. For additional technical support, please contact Ascent Research.
