The KNOP1 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the KNOP1 gene in a human hepatic adenocarcinoma background. This product is generated by CRISPR/Cas9-mediated gene disruption in the SK-HEP-1 host cell line, yielding a heterogeneous pool of cells with targeted ablation of KNOP1 expression, suitable for investigating nucleolar biology and ribosome biogenesis in liver cancer models.
The SK-HEP-1 cell line was originally established from the ascitic fluid of a patient with liver adenocarcinoma and serves as a widely used in vitro model for hepatocellular carcinoma (HCC). These cells exhibit an epithelial morphology and retain metastatic potential when introduced into xenograft models, making them a relevant system for dissecting HCC tumor biology, including cell proliferation, migration, and metastatic dissemination.
KNOP1 is a nucleolar protein that functions as a critical regulator of pre-rRNA processing, ribosome biogenesis, and nucleolar structural integrity, ultimately influencing cellular protein synthesis capacity and proliferation. Mechanistically, KNOP1 operates downstream of the mTORC1 and c-Myc signaling pathways, which couple nutrient and growth signals to ribosome production. It interacts directly with nucleolar components such as nucleophosmin (NPM1), the NOP56/58 complex, and fibrillarin to facilitate early rRNA cleavage events. Knockout of KNOP1 is expected to interrupt ribosomal subunit maturation, leading to nucleolar stress and potential activation of the p53 pathway, resulting in cell cycle arrest or apoptosis.
Within the SK-HEP-1 hepatocellular carcinoma context, disruption of KNOP1 provides a powerful tool to dissect the role of ribosome biogenesis in liver cancer pathogenesis. Aberrantly elevated ribosome production is a hallmark of many cancers, including HCC, and KNOP1 depletion can help elucidate how nucleolar stress impacts tumor cell growth, survival, and invasive properties. This model enables the investigation of whether compromised ribosome assembly sensitizes liver cancer cells to mTOR inhibitors or chemotherapeutic agents targeting translation, thus informing therapeutic strategies for HCC.
This polyclonal knockout population is well-suited for a broad range of downstream applications, including Western blotting for ribosomal protein levels, RT-qPCR profiling of pre-rRNA processing intermediates, transcriptomic analysis via RNA-seq, and immunofluorescence-based assessment of nucleolar morphology. Furthermore, the cells can be employed in functional assays such as MTT/CCK-8 proliferation measurements, flow cytometric cell cycle analysis, and migration/invasion studies to evaluate the phenotypic consequences of KNOP1 loss in a metastatic HCC background. For additional technical details, protocols, or pricing inquiries, please contact Ascent Research.
