The KDM5B Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 143B osteosarcoma cell line, engineered to disrupt the KDM5B gene. This loss-of-function model enables the study of KDM5B-dependent epigenetic regulation and its contributions to oncogenic processes. The polyclonal nature of this product provides a heterogeneous pool of gene-edited cells, capturing a range of knockout events that collectively abolish KDM5B function, making it suitable for population-based functional assays.
The host 143B cell line is a widely utilized human osteosarcoma model, originally derived from a malignant bone tumor. These mesenchymal cells retain key features of osteosarcoma, including aggressive proliferative capacity and metastatic potential, and are extensively employed in bone cancer and metastasis research. The 143B background offers a clinically relevant platform for investigating molecular mechanisms underlying osteosarcoma progression and for evaluating therapeutic interventions.
KDM5B (also known as JARID1B or PLU-1) encodes a histone lysine demethylase that specifically removes di- and trimethyl groups from histone H3 at lysine 4 (H3K4me2/3), thereby mediating chromatin compaction and transcriptional repression of target loci. Its activity is regulated by upstream factors including MYC, retinoic acid receptors (RAR/RXR), estrogen receptor alpha, and miR-137. KDM5B forms repressive complexes with PRC1/2, HDAC1/2, SIN3A, DNMTs, and the NuRD complex. Key downstream targets include HOX gene clusters, CDKN1A (p21), Cyclin D1, E-cadherin, and BRCA1. Through H3K4 demethylation, KDM5B modulates pathways central to stem cell pluripotency, retinoic acid signaling, and epigenetic silencing.
In the context of osteosarcoma, KDM5B is frequently deregulated and contributes to tumorigenesis by sustaining stem cell-like properties, promoting proliferation, and facilitating drug resistance. The 143B knockout model allows researchers to dissect how loss of KDM5B-mediated H3K4 demethylation impacts malignant phenotypes, including metastatic behavior and sensitivity to chemotherapeutics. Given KDM5B??s documented roles in intellectual disability, autism spectrum disorder, and various cancers such as breast cancer, melanoma, and leukemia, this model also holds broader translational relevance.
Applications of the KDM5B Knockout 143B Polyclonal Cells span epigenetic regulation studies, cancer biology, drug resistance mechanism investigation, and stem cell differentiation research. Typical assays include Western blotting for KDM5B and histone modification levels, RT-qPCR for target gene expression changes, ChIP-qPCR to assess H3K4me3 enrichment, and RNA-seq for transcriptome-wide profiling. Functional readouts such as MTT/CCK-8 proliferation assays, migration and invasion tests, and Annexin V/PI apoptosis assays enable phenotypic characterization. Additionally, these cells are amenable to high-throughput drug sensitivity screening to identify KDM5B-dependent vulnerabilities. For further information or to discuss custom applications, please contact Ascent Research.
