The KDM5C Knockout 143B Polyclonal Cells product comprises a population of human osteosarcoma 143B cells subjected to CRISPR/Cas9-mediated disruption of the KDM5C gene. This polyclonal knockout pool introduces loss-of-function mutations across the cell population, enabling the study of KDM5C-dependent functions without clonal isolation. The polyclonal format preserves heterogeneous editing outcomes, which may better represent the diversity of genetic alterations in tumor contexts. By ablating KDM5C expression, researchers can interrogate its role in chromatin regulation and transcriptional control.
The 143B cell line is a well-established human osteosarcoma model derived from HOS cells. These mesenchymal-origin cells exhibit aggressive growth properties and are widely employed in bone cancer research. 143B cells harbor mutations that drive malignancy, making them a relevant system for dissecting tumorigenic pathways. The osteosarcoma background provides a clinically pertinent environment to assess how KDM5C disruption influences cancer cell behavior, including proliferation, migration, and metastatic potential.
KDM5C encodes a histone H3K4 demethylase that specifically removes di- and trimethyl groups from lysine 4 of histone H3 (H3K4me2/me3), leading to transcriptional repression. It functions within larger multiprotein complexes, including the REST corepressor complex, and interacts with HDAC1/2 and SIN3A. KDM5C is recruited to chromatin by the REST transcription factor, and its enzymatic activity is modulated by neuronal activity signals and potentially by ERK/MAPK signaling. Downstream, KDM5C regulates genes involved in neuronal function and cancer-related processes by modifying local H3K4 methylation landscapes. Knockout of KDM5C thus perturbs these repressive complexes and derepresses target genes.
In the 143B osteosarcoma context, loss of KDM5C is expected to alter the epigenetic landscape, potentially affecting the expression of tumor suppressor genes and oncogenes. Given the role of KDM5C in neurodevelopmental disorders such as X-linked intellectual disability and autism spectrum disorder, this model also serves as a platform to study the molecular underpinnings of these conditions. The disruption of KDM5C-mediated chromatin remodeling may impact cell cycle progression, apoptosis, and differentiation, offering insights into osteosarcoma pathogenesis and therapeutic vulnerabilities.
This knockout model is suitable for a variety of research applications, including epigenetic regulation studies, cancer epigenetics, and functional genomics screening. Researchers can employ ChIP-qPCR to assess H3K4me3 enrichment at specific loci, RNA-seq to profile transcriptomic changes, and western blotting to monitor global histone methylation alterations. Phenotypic assays such as cell viability, migration/invasion, and colony formation enable functional characterization of KDM5C in osteosarcoma biology. For additional information and technical support, please contact Ascent Research.
