The JADE3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered for loss-of-function studies of the JADE3 gene in a human cervical adenocarcinoma model. This polyclonal population is generated by CRISPR/Cas9-mediated disruption of the JADE3 locus, creating a heterogeneous editing profile that avoids clonal selection and more closely mimics the variability observed in pooled genetic screens and tumor cell populations. It is well-suited for high-throughput epigenetic drug screening and detailed mechanistic investigations of chromatin regulation and cell proliferation.
The parental HeLa cell line is an HPV18-positive epithelial line derived from a cervical adenocarcinoma. Its immortalized phenotype results from viral oncoprotein-mediated inactivation of the tumor suppressors p53 and Rb, leading to dysregulated cell cycle and apoptosis. HeLa cells are extensively characterized and widely employed in cancer biology research, providing a robust and relevant background for examining epigenetic modifiers such as JADE3 in the context of oncogenic transformation.
JADE3 encodes a PHD finger scaffold protein that specifically recognizes trimethylated histone H3 at lysine 4 (H3K4me3) and nucleates the assembly of the HBO1 (KAT7) acetyltransferase complex. This complex includes the cofactors ING4 or ING5, MEAF6, and BRPF1, and is recruited by JADE3 to chromatin regions marked by H3K4me3. Once bound, the complex acetylates histone H3 at K9 and K14 and histone H4 at K5 and K12, leading to chromatin relaxation and transcriptional activation of downstream targets such as Cyclin D1 and MYC. JADE3 expression is itself regulated by growth factor signaling cascades and transcription factors including SP1 and MYC, and it participates in Wnt signaling, placing it at a critical intersection of mitogenic and epigenetic control.
In the HeLa context, disruption of JADE3 allows dissection of its role in maintaining the acetylated chromatin landscape that drives uncontrolled proliferation. Dysregulation of JADE3 has been implicated in lung adenocarcinoma and breast cancer, and it is also associated with neurodevelopmental disorders, underscoring its broad biological significance. By abrogating JADE3 function in an HPV-driven, p53/Rb-deficient background, researchers can evaluate how loss of histone acetylation at specific loci alters oncogenic gene expression programs and can probe compensatory chromatin remodeling mechanisms.
This polyclonal knockout product is ideal for numerous applications, including epigenetic drug screening to assess sensitivity to histone deacetylase or bromodomain inhibitors. Biochemical assays such as ChIP-qPCR enable quantitative measurement of changes in histone acetylation marks (H3K9ac, H3K14ac), while Western blotting and RT-qPCR can monitor effector proteins and transcripts like Cyclin D1 and MYC. Functional readouts of proliferation (MTS, BrdU) and colony formation provide additional layers of phenotypic validation. The heterogeneous knockout population offers a realistic model for tumor cell dynamics in drug response studies. For technical inquiries and ordering information, please contact Ascent Research.
