The JADE1 knockout SK-HEP-1 polyclonal cells are a CRISPR/Cas9-edited population of human SK-HEP-1 cells with targeted disruption of the JADE1 gene. This polyclonal knockout product consists of a heterogeneous pool of cells, each bearing independent loss-of-function mutations, providing a robust model to study JADE1 ablation without clonal selection bias. It is intended for investigations into JADE1??s roles in epigenetic regulation, cell cycle control, and tumor suppression within a hepatic cancer background.
The parental SK-HEP-1 cell line is an epithelial line originally derived from the ascites of a 52-year-old male with liver adenocarcinoma. Widely used as a hepatocellular carcinoma (HCC) model, SK-HEP-1 displays adherent growth and tumorigenic properties suitable for in vitro studies of invasion, migration, and drug response, as well as xenograft experiments.
JADE1 (PHF17) is a scaffold protein that assembles the HBO1 (KAT7) histone acetyltransferase complex, which includes ING4/5 and EAF6. This complex acetylates histone H4, particularly at replication origins, to facilitate DNA replication and transcription. JADE1 also functions as a substrate recognition subunit for the VHL ubiquitin ligase, connecting epigenetic regulation to proteasomal degradation and oxygen sensing. Through these interactions, JADE1 regulates genes such as cyclin D1 and controls G1/S cell cycle progression, while also interacting with E2F1 in DNA damage responses.
In SK-HEP-1 HCC cells, JADE1 knockout is expected to diminish HBO1-dependent histone H4 acetylation, altering transcriptional networks that govern proliferation and apoptosis. Given JADE1??s putative tumor suppressor activity in renal clear cell carcinoma and acute myeloid leukemia, this model enables dissection of JADE1-dependent pathways in liver cancer. The VHL-JADE1-HBO1 axis links oxygen sensing to chromatin dynamics, offering a platform to study how disruption of this pathway fuels hepatocarcinogenesis and identifies therapeutic targets.
These polyclonal knockout cells support applications in epigenetic profiling, cell cycle analysis, and drug target validation. Assays such as ChIP-qPCR for histone marks, flow cytometry for cell cycle and apoptosis, and co-immunoprecipitation for complex assembly are readily performed. The model is also amenable to drug sensitivity screens, migration assays, and signaling studies using western blotting and RT-qPCR. For further information and support, please contact Ascent Research.
