The KDM5B Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human MCF-7 breast adenocarcinoma cell line. This product features targeted disruption of KDM5B, encoding an H3K4me1/2/3 demethylase. The polyclonal pool preserves genetic heterogeneity from CRISPR/Cas9 editing, providing a robust loss-of-function model suitable for population-based analyses.
The MCF-7 host cell line is a well-established model of estrogen receptor-positive (ER+) human breast adenocarcinoma, originally isolated from the pleural effusion of a female patient with metastatic disease. These adherent epithelial cells retain functional estrogen receptor alpha (ESR1) signaling and are widely employed in breast cancer research to study hormone-responsive transcriptional networks, endocrine resistance, and tumor biology. The MCF-7 background provides a relevant context for interrogating KDM5B function in luminal-type breast cancer, where histone methylation dynamics influence gene expression programs critical for proliferation and differentiation.
KDM5B functions as a transcriptional repressor by demethylating H3K4me1/2/3, removing activating chromatin marks to promote a repressive state. In MCF-7 cells, its expression is regulated by MYC, E2F factors, ESR1, and miR-137. KDM5B associates with HDAC1/2, the NuRD complex (MTA1/MTA2), and EZH2 to silence targets such as CDKN1A (p21), CDKN1B (p27), BBC3, BRCA1, and HOX genes. This network links KDM5B to RB1, E2F1, MYC, H3K4me3, and H3K9ac.
Disruption of KDM5B in the MCF-7 background is predicted to relieve transcriptional repression of tumor suppressor and cell cycle regulatory genes, potentially restoring growth-inhibitory programs and sensitizing cells to apoptotic stimuli. Given the central role of ESR1 signaling in this cell line, KDM5B knockout may also impact estrogen-dependent transcription, offering a tool to dissect epigenetic regulation of hormone receptor activity. This model is particularly relevant for investigating luminal B breast cancer, where KDM5B overexpression correlates with aggressive phenotypes, as well as for exploring mechanisms of resistance to endocrine therapies.
Researchers can utilize this knockout model in a variety of experimental contexts, including breast cancer epigenetic studies, screening of small-molecule KDM5B inhibitors, and dissection of transcriptional regulatory networks. Representative assays include Western blotting for global H3K4me3 levels, RT-qPCR to assess derepression of CDKN1A and BRCA1, and chromatin immunoprecipitation (ChIP-qPCR) to monitor H3K4me3 enrichment at target gene promoters. Additional applications involve cell proliferation and apoptosis assays, as well as drug sensitivity profiling to evaluate combination therapies. For further details or technical support, please contact Ascent Research.
