The JADE2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the JADE2 locus, enabling loss-of-function studies of the JADE2 transcriptional coactivator. The polyclonal format preserves genetic diversity while eliminating wild-type JADE2 expression, allowing researchers to assess the functional impact of JADE2 deficiency across a population of cells. This model is ideal for investigating JADE2-dependent gene regulation and its role in colorectal cancer biology without clonal selection artifacts.
The HT29 cell line originates from a human colorectal adenocarcinoma of a female patient, featuring a mutant p53 tumor suppressor and the capacity for enterocytic differentiation upon appropriate stimuli. As a well-characterized model of intestinal epithelial carcinoma, HT29 cells display aberrant Wnt/??-catenin signaling and a stem-like phenotype, making them highly relevant for studying mechanisms of colorectal tumorigenesis and cancer stem cell maintenance. Their epithelial origin and differentiation potential further enable research into the interplay between epigenetic regulation and tumor cell plasticity.
JADE2 is a scaffold protein within the HBO1 (KAT7) histone acetyltransferase complex, which also includes ING4/ING5 and MEAF6. This complex is recruited to gene promoters through recognition of histone H3 trimethylated at lysine 4 (H3K4me3) marks, where it acetylates histone H4, thereby promoting transcriptional activation. JADE2 functions downstream of TCF/LEF transcription factors activated by Wnt signaling and is influenced by EGFR signaling pathways. Consequently, JADE2 transduces these upstream signals to the transcriptional activation of critical Wnt target genes such as MYC, CCND1, AXIN2, and LGR5, which drive cell proliferation and stemness. The physical interaction of JADE2 with HBO1, ING4/ING5, and MEAF6 forms the core of a chromatin-remodeling module that links epigenetic marks to oncogenic transcription.
In the context of HT29 cells with mutant p53 and hyperactive Wnt signaling, JADE2 likely sustains the expression of genes essential for tumor cell growth and maintenance of cancer stem cell properties. Disruption of JADE2 in this background allows researchers to dissect its specific contributions to epigenetic-driven oncogenic programs, independent of clonal variation. This knockout model is particularly suited for exploring how JADE2-dependent histone acetylation impacts Wnt-regulated phenotypes such as self-renewal, differentiation, and drug sensitivity in colorectal adenocarcinoma cells.
The JADE2 Knockout HT29 Polyclonal Cells are suited for a broad range of experimental applications, including epigenetic studies of histone acetylation dynamics, investigations of Wnt/??-catenin target gene regulation, and functional genomics screening for novel therapeutic targets. Researchers can perform Western blotting to confirm loss of JADE2 and downstream effectors, RT-qPCR to quantify Wnt target gene expression, and ChIP-qPCR to assess H4 acetylation changes at specific promoters. Stem cell phenotypes can be evaluated by flow cytometry for CD44 and CD133 expression, while cellular behavior phenotypes can be characterized using proliferation and migration assays. Co-immunoprecipitation experiments can probe the integrity of the HBO1 complex, and Wnt reporter assays combined with drug sensitivity profiling enable the study of signaling pathway dependencies and therapeutic vulnerabilities. For additional information or technical support, please contact Ascent Research.
