The DPCD Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 host cell line, engineered for targeted disruption of the DPCD gene. This polyclonal product provides a heterogeneous mixture of gene-edited cells, enabling functional studies without the bias of clonal selection. The knockout was achieved using CRISPR/Cas9-mediated gene disruption, generating a reliable loss-of-function model for DPCD. The polyclonal format ensures representation of diverse editing outcomes, supporting robust phenotypic analysis in downstream applications.
The SK-HEP-1 cell line is a human hepatic adenocarcinoma line derived from ascitic fluid of a 52-year-old male patient. It serves as a classic model for liver cancer research, exhibiting epithelial morphology and aggressive growth characteristics. SK-HEP-1 cells are extensively used to study tumor cell invasion, metastasis, and signaling pathways in hepatocellular carcinoma. Their amenability to gene editing and reproducible culture conditions make them an ideal host for generating knockout derivatives.
DPCD is a ciliary protein essential for proper axonemal architecture and motile cilia function. Upstream transcription factors RFX and FOXJ1 regulate DPCD expression, while DPCD interacts with dynein arm components DNAI1 and DNAH5, as well as intraflagellar transport (IFT) complexes. Loss of DPCD disrupts ciliary motility and compromises Hedgehog signaling, likely through impaired processing of GLI transcription factors. This positions DPCD at the intersection of ciliary mechanics and Hh pathway transduction, critical for tissue homeostasis and developmental processes.
In the SK-HEP-1 hepatic adenocarcinoma context, DPCD knockout enables investigation of ciliary contributions to liver cancer biology. Aberrant Hedgehog signaling is associated with liver cancer progression, and ciliary dysfunction may further alter tumor cell behavior. This model provides a unique tool to dissect how cilia influence proliferation, migration, and drug response in hepatic tumors, potentially revealing novel therapeutic targets. It allows evaluation of ciliary loss on oncogenic phenotypes such as invasion and chemosensitivity.
Researchers can employ this polyclonal population for diverse applications, including ciliary biology studies, primary ciliary dyskinesia research, and drug screening for ciliopathies. Standard assays include western blotting to confirm DPCD knockout, immunofluorescence for cilia markers like acetylated tubulin, and RT-qPCR for ciliary gene expression. Functional assays such as transwell migration/invasion and cell viability tests assess phenotypic consequences. These cells also serve as a platform to explore Hedgehog pathway crosstalk in liver cancer. For further information, please contact Ascent Research.
