The CCPG1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated for functional analysis of the CCPG1 gene in a human hepatic adenocarcinoma background. This heterogeneous pool of loss-of-function mutants allows for unbiased assessment of CCPG1-dependent phenotypes in cell cycle regulation and DNA damage response. The polyclonal format is particularly suited for pooled screening studies, providing a robust starting point for investigating tumor suppressor mechanisms in liver cancer.
The SK-HEP-1 host cell line, derived from the ascites of a male liver adenocarcinoma patient, exhibits adherent epithelial morphology and is extensively employed as a model for hepatocellular carcinoma, liver metabolism, and drug metabolism. Its hepatic characteristics make it an appropriate context for studying how disruption of CCPG1-mediated signaling impacts tumor cell proliferation and survival.
CCPG1 operates as a critical downstream effector of the p53 (TP53) tumor suppressor pathway. It is transcriptionally activated by p53 following DNA damage and physically interacts with the COP9 signalosome, notably the COPS5/JAB1 subunit, to modulate ubiquitin-dependent proteolysis. This interaction promotes the stabilization of CDKN1A (p21) and inhibition of cyclin-dependent kinases, thereby enforcing cell cycle arrest. The signaling axis involves upstream kinases such as ATM and regulators like MDM2, placing CCPG1 at a convergence point between genotoxic stress sensing and proteasomal control of cell growth.
In the context of hepatocellular carcinoma, loss of CCPG1 function may disable critical growth-suppressive checkpoints, contributing to unchecked proliferation and resistance to apoptosis. The SK-HEP-1 knockout model thus provides a valuable tool to dissect the tumor-suppressive role of CCPG1 in liver cancer, enabling detailed studies of cell cycle progression, drug sensitivity, and DNA repair mechanisms. Comparative analyses with wild-type cells can uncover vulnerabilities specific to CCPG1-deficient tumors.
This product is ideal for applications such as flow cytometry-based cell cycle analysis, Annexin V apoptosis assays, and co-immunoprecipitation to probe CCPG1 interactions with COP9 signalosome components and p53. Drug sensitivity testing with genotoxic chemotherapeutics or targeted agents can reveal altered chemo-responsiveness, while RT-qPCR and Western blotting validate transcriptional and protein-level changes. For further information, please contact Ascent Research.
