The CCDC14 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 hepatocellular carcinoma cell line, featuring disruption of the CCDC14 gene. This loss-of-function model allows investigation of CCDC14 ablation in a liver cancer context while preserving the heterogeneity inherent to polyclonal editing.
The Huh-7 cell line originates from a well-differentiated hepatocellular carcinoma of a 57-year-old Japanese male. Widely used in liver cancer research, Huh-7 cells retain hepatocyte-like characteristics and serve as a robust model for studying tumorigenesis, metastasis, and drug response.
CCDC14 is a coiled-coil domain protein that localizes to the centrosome and interacts with CEP63 to facilitate centriole duplication. It acts downstream of PLK4 and regulates assembly of centriole components SAS-6, STIL, and CPAP, while its activity is modulated by CDK2 and Aurora A. CCDC14 thus orchestrates critical steps in centrosome duplication, and its dysfunction leads to centrosome amplification, genomic instability, and potential carcinogenesis.
In Huh-7 hepatocellular carcinoma cells, CCDC14 knockout provides a disease-relevant model to examine how centrosome defects promote liver carcinogenesis. Centrosome amplification is prevalent in HCC and associated with chromosomal instability. This polyclonal knockout population enables dissection of altered centrosome regulation, ciliogenesis defects, and cell cycle checkpoint disruption underlying HCC progression.
Applications include investigating centrosome duplication and ciliogenesis mechanisms, studying cell cycle dysregulation in HCC, and screening anti-cancer compounds that target centrosome amplification. Compatible assays encompass immunofluorescence for gamma-tubulin and centrin, western blotting of CCDC14, CEP63, and cell cycle proteins, flow cytometry for cell cycle and ploidy, MTT/BrdU proliferation assays, migration/invasion assays, and RNA-seq. For inquiries, contact Ascent Research.
