The KDM2B Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma line, designed for loss-of-function interrogation of KDM2B. This polyclonal pool harbors heterogeneous CRISPR-mediated disruptions of the target locus, enabling population-level studies of KDM2B-dependent phenotypes without single-cell cloning artifacts. The model is optimized for transient and stable assays in epigenetics, oncology, and signal transduction, providing a reproducible system to dissect KDM2B biology in an intestinal epithelial background.
HT29 cells are epithelial adherent cells originally isolated from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female. They carry mutant p53 and are capable of forming polarized monolayers with tight junctions, making them a well-established model for colon cancer biology, intestinal barrier function, and drug transport studies. Their tumorigenic nature and widespread use in preclinical oncology research render them an appropriate host for investigating epigenetic regulators implicated in colorectal tumorigenesis.
KDM2B encodes a histone lysine demethylase that specifically removes methyl groups from H3K4 and H3K36, thereby modulating transcriptional activation and elongation. As a core component of the non-canonical polycomb repressive complex 1.1 (ncPRC1.1), it partners with BCOR, PCGF1, RING1, and RYBP to catalyze histone H2A ubiquitination, promoting gene silencing at developmental loci and tumor suppressor genes such as CDKN1A and CDKN2A. KDM2B is transcriptionally activated by MYC and CTNNB1 and integrates signals from the Wnt and NF-??B pathways, as evidenced by its regulation by NFKB1 and HIF1A. It reciprocally controls expression of downstream effectors including NANOG, SOX2, MYC, and CCND1, linking chromatin modification to cell cycle progression and stemness. Additionally, KDM2B physically interacts with SKP1, CUL1, RB1, E2F1, and HDAC1, embedding it within ubiquitination, cell cycle regulatory, and chromatin remodeling networks.
In the HT29 colorectal adenocarcinoma context, KDM2B is frequently associated with poor prognostic features, making its knockout a powerful tool to examine epigenetic drivers of colon cancer. This model allows dissection of how KDM2B-mediated H3K4/H3K36 demethylation and ncPRC1.1-dependent repression influence malignant phenotypes such as aberrant proliferation, senescence bypass, and invasion. Given the intact Wnt signaling axis (CTNNB1, TCF4, LEF1) and NF-??B activity in HT29 cells, researchers can explore how KDM2B loss perturbs these interconnected pathways and alters tumorigenic properties, including drug transporter expression and chemosensitivity.
This polyclonal knockout product supports diverse applications including colorectal cancer epigenetics, ncPRC1.1 characterization, and drug response profiling. It is compatible with western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, immunofluorescence, and flow cytometry for molecular analysis, as well as colony formation, wound healing, transwell invasion, and MTT assays for phenotypic readouts. Co-immunoprecipitation experiments can validate KDM2B-containing complexes. The model is well-suited for gene expression profiling and cell cycle/senescence studies in a tumorigenic intestinal background. For further information, please contact Ascent Research.
