CCDC97 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 human hepatocellular carcinoma cell line, engineered for loss-of-function studies of the CCDC97 gene. This polyclonal product offers a heterogeneous population of gene-disrupted cells, suitable for investigating CCDC97’s role in liver cancer biology without clonal isolation bias. The knockout model provides a versatile tool for dissecting tumor suppressor mechanisms in a well-characterized hepatic background.
The parental Huh-7 cell line originates from a well-differentiated hepatocellular carcinoma of a 57-year-old Japanese male and is widely employed in hepatic biology, oncology, and drug metabolism research. These adherent epithelial cells retain hepatocyte-like features, including expression of liver-specific markers and susceptibility to hepatitis C virus replication, making them a standardized platform for modeling HCC in vitro. The CCDC97 knockout in this line allows direct interrogation of gene function in a clinically relevant liver cancer context.
CCDC97 encodes a coiled-coil domain-containing protein proposed to act as a tumor suppressor in hepatocellular carcinoma. Its coiled-coil domain likely mediates protein?Cprotein interactions essential for regulating cell cycle progression and apoptosis, though specific binding partners remain to be identified. Disruption of CCDC97 is hypothesized to deregulate key signaling nodes, including Cyclin D1 for cell cycle control, the Bcl-2 family for apoptotic balance, and ??-catenin within the Wnt pathway. Loss of CCDC97 function may therefore promote unchecked proliferation and resistance to cell death, contributing to hepatocarcinogenesis.
In Huh-7 cells, a line established from a human HCC, CCDC97 knockout recapitulates the gene’s putative inactivation observed in some liver tumors. This model enables dissection of CCDC97-dependent mechanisms driving HCC progression, including aberrant cell cycle entry and evasion of apoptosis. Since Huh-7 cells harbor wild-type p53 and other relevant oncogenic alterations, the knockout provides a clean background to assess how CCDC97 loss interacts with existing tumorigenic pathways. The system is particularly valuable for studying how coiled-coil domain-mediated interactions integrate signals to suppress transformation, and for validating CCDC97 as a potential biomarker or therapeutic target.
Researchers can employ these polyclonal knockout cells for a broad range of functional assays, such as cell viability and colony formation studies to evaluate growth advantages, migration/invasion assays to assess metastatic potential, and Western blotting for apoptosis markers like cleaved caspases or Bcl-2 family members. RNA-seq transcriptome profiling can reveal downstream transcriptional changes upon CCDC97 loss, while drug sensitivity screens can identify synthetic lethal interactions or resistance mechanisms. Additionally, the polyclonal nature allows analysis of heterogeneous knockout effects, simulating tumor heterogeneity. For technical inquiries or custom cell line engineering, please contact Ascent Research.
