KDM5B Knockout KYSE-30 Polyclonal Cells are a pooled population of KYSE-30 cells subjected to CRISPR/Cas9-mediated disruption of the KDM5B locus. This polyclonal knockout product generates a heterogeneous loss-of-function model suitable for studying KDM5B-dependent processes in an esophageal cancer context. The product is supplied as viable polyclonal cells ready for expansion and downstream assays.
The host cell line, KYSE-30, was established from a poorly differentiated invasive esophageal squamous cell carcinoma of the middle thoracic esophagus from a 64-year-old male patient. This cell line is extensively characterized and serves as a robust in vitro model for studying aggressive esophageal cancer phenotypes, including proliferation, invasion, and drug resistance.
KDM5B acts as a transcriptional repressor by demethylating histone H3 lysine 4 trimethylation (H3K4me3) at promoter regions, thereby silencing tumor suppressor genes such as CDKN1A, BAX, and BRCA1. Its activity is regulated by upstream factors including E2F transcription factors, MYC, and the TGF-?? pathway, while it interacts with epigenetic complexes like Sin3A-HDAC, NuRD, and PRC2 to coordinate gene silencing. Through these interactions, KDM5B modulates downstream effectors in the Wnt, Notch, and PI3K/AKT pathways, influencing cell cycle progression, apoptosis, and epithelial-mesenchymal transition.
In the KYSE-30 esophageal squamous cell carcinoma model, KDM5B disruption provides a powerful tool to dissect its role in tumor aggressiveness. Given the cell line’s origin from a poorly differentiated invasive tumor, the polyclonal knockout population enables researchers to evaluate how loss of KDM5B impacts proliferation, migration, and survival in a background harboring native oncogenic drivers. This model is particularly relevant for investigating the interplay between KDM5B-mediated epigenetic silencing and key pathways such as p53 and Wnt signaling in esophageal carcinogenesis.
Typical applications include assessing KDM5B’s effect on cell proliferation using MTS/CCK8 and colony formation assays, measuring apoptosis by Annexin V staining, and analyzing cell cycle distribution via flow cytometry. The cells are also suited for invasion and migration assays to study metastatic potential, ChIP-qPCR to examine changes in H3K4me3 occupancy at target gene promoters, and transcriptomic analysis by RNA-seq. Additionally, the polyclonal population can be used in xenograft models to evaluate tumorigenicity and drug response in vivo. For technical inquiries and ordering, please contact Ascent Research.
