The JMJD7 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the JMJD7 gene in the human hepatic adenocarcinoma SK-HEP-1 cell line. This non?clonal polyclonal pool, generated via CRISPR/Cas9-mediated gene disruption, provides a loss-of-function model that abrogates JMJD7 protein expression across a heterogeneous cell population. The cells serve as a robust platform for dissecting JMJD7-dependent mechanisms in cancer biology without the limitations of single?cell clones.
The SK-HEP-1 host cell line, established from the ascites of a patient with hepatic adenocarcinoma, is a widely used model for hepatocellular carcinoma and liver adenocarcinoma research. These cells retain key malignant properties including rapid proliferation and invasive capacity, and they are extensively characterized for studies of liver cancer signaling, drug response, and metastasis. This background offers a physiologically relevant context for exploring the functional roles of JMJD7 in hepatic tumor biology.
JMJD7 encodes a JmjC domain-containing oxygenase with dual roles: putative histone demethylase activity and ribosomal oxygenase function. It interacts directly with ribosomal protein L8 (RPL8) and depends on cofactors 2?oxoglutarate, Fe2?, and oxygen. Transcription of JMJD7 is regulated by upstream factors HIF1A, MYC, and SP1, placing it within hypoxia signaling and oncogenic stress pathways. Downstream, JMJD7 catalyzes demethylation of histone H3K9me2, influencing chromatin structure and gene expression, and hydroxylates RPL8, impacting ribosome biogenesis and translation. These activities link epigenetic modification to translational control.
In the SK-HEP-1 hepatic adenocarcinoma context, disruption of JMJD7 is anticipated to perturb histone methylation patterns and ribosomal protein hydroxylation, leading to altered gene expression programs and translational output. Such changes may affect tumor cell proliferation, survival, migration, and metabolic adaptation. The polyclonal knockout pool minimizes clonal artifacts and better mirrors tumor heterogeneity, enhancing the translational relevance of functional studies in liver cancer.
These polyclonal knockout cells are suitable for diverse applications: Western blotting and RT?qPCR for knockout validation, ChIP?qPCR and immunofluorescence to assess histone H3K9me2 modifications, and proliferation, migration, and invasion assays to evaluate tumorigenic properties. Transcriptomic profiling via RNA?seq can identify JMJD7?regulated gene networks. Additionally, metabolic assays, phospho?signaling analysis, and drug sensitivity screening enable assessment of JMJD7 as a therapeutic target. For technical inquiries, please contact Ascent Research.
