The KDM5B Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, providing disruption of the KDM5B gene in the HCT 116 human colorectal carcinoma cell line. This polyclonal model is ideal for functional studies of epigenetic silencing in colorectal cancer, avoiding clonal selection artifacts.
HCT 116 cells are an extensively used colorectal carcinoma line with activating KRAS (G13D) and inactivating TP53 mutations, reflecting common genetic drivers of disease. Their epithelial origin and robust growth make them a standard platform for cancer research, drug development, and xenograft assays.
KDM5B encodes a histone H3K4me2/3 demethylase that functions as a transcriptional repressor. It is regulated by MYC, E2F, and retinoic acid signaling, and interacts with HDAC1/2, REST, SIN3A, and the NuRD complex to silence tumor suppressors like CDKN1A (p21) and HOX genes. KDM5B also represses Wnt target genes and differentiation programs, linking chromatin remodeling to oncogenic pathways.
In HCT 116, KDM5B knockout elevates H3K4me3 at target promoters, derepressing tumor suppressor genes and reducing cell proliferation, colony formation, and tumorigenicity in vivo. This model thus illuminates epigenetic mechanisms driving colorectal cancer and offers a platform for studying differentiation therapy.
Applications include western blotting for KDM5B and histone marks, RT-qPCR and RNA-seq for transcriptome analysis, ChIP-qPCR for H3K4me3 occupancy, and functional assays such as proliferation, colony formation, and xenograft tumor models. Drug sensitivity studies with KDM5B inhibitors can also be performed. For additional details, contact Ascent Research.
