The KIFC3 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the SK-HEP-1 host, engineered for targeted disruption of the KIFC3 gene. This loss-of-function model, generated via CRISPR/Cas9-mediated gene targeting, provides a heterogeneous knockout pool that preserves the genetic diversity of a non-clonal population, making it suitable for a broad range of functional analyses without clonal selection bias.
The SK-HEP-1 host cell line is an ascites-derived human hepatic adenocarcinoma model that recapitulates key biological features of liver adenocarcinoma. This well-characterized line exhibits aberrant mitotic regulation and serves as a clinically relevant system for examining the roles of mitotic motors and ciliary proteins in tumor biology.
KIFC3 encodes a minus-end-directed kinesin motor protein that localizes to spindle poles and ciliary axonemes, where it is essential for mitotic spindle organization, chromosome alignment, and intraflagellar transport. The protein functions downstream of regulatory inputs from FOXM1, E2F transcription factors, and cyclin-dependent kinases, and interacts with microtubules, dynein, dynactin, importin ??, and katanin. In mitosis, KIFC3 cooperates with NUMA and TPX2 to focus spindle poles, acting within a pathway that includes PLK1 and Aurora A, while in cilia it is linked to IFT88-mediated transport. Disruption of KIFC3 impairs spindle integrity and ciliogenesis, leading to chromosomal misalignment and potential polyploidy.
In the SK-HEP-1 liver adenocarcinoma context, loss of KIFC3 is predicted to compromise mitotic fidelity, resulting in altered proliferation, increased genomic instability, and modified sensitivity to microtubule-targeting agents. Additionally, because ciliary dysfunction is increasingly implicated in tumor progression and drug resistance, this model provides insights into ciliopathy-associated mechanisms relevant to hepatocellular carcinoma and polycystic kidney disease.
This polyclonal knockout cell product enables detailed investigation of mitotic spindle regulation via immunofluorescence and live-cell imaging, functional screening of mitotic inhibitors using flow cytometry and viability assays, and transcriptomic profiling by RNA-seq. Applications include characterizing polyploidy, genomic instability, and ciliogenesis in liver adenocarcinoma. Common assays comprise western blotting for targets such as NUMA and TPX2, drug sensitivity testing, and proliferation analyses. For further information, please contact Ascent Research.
