The KDM5D Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from MCF-7 human breast adenocarcinoma cells, characterized by disruption of the KDM5D gene. As a polyclonal knockout pool, the cells contain a diverse array of editing events, avoiding clonal bias and better reflecting intratumoral heterogeneity. This model is provided as a live cell product suitable for immediate expansion and experimentation, and it is designed for researchers requiring a loss-of-function system without the limitations of single-cell-derived clones.
MCF-7 cells were isolated from the pleural effusion of a 69-year-old Caucasian woman with metastatic breast adenocarcinoma and are a classic estrogen receptor-positive, hormone-responsive model. These adherent epithelial cells express both estrogen and progesterone receptors, and their proliferation is stimulated by estrogen, making them a standard platform for studying hormone-dependent breast cancer. Their well-documented signaling networks and genotypic stability make MCF-7 an ideal host for gene editing studies focused on endocrine-responsive malignancies.
KDM5D encodes a Jumonji C-domain histone demethylase that specifically erases di- and trimethylation of histone H3 lysine 4 (H3K4me2/3), a mark associated with active transcription. Thus, KDM5D acts as a potent transcriptional repressor. Its expression is regulated upstream by the androgen receptor and the transcription factor SOX9. In the nucleus, KDM5D interacts with chromatin remodeling complexes and Polycomb repressive complex 2 (PRC2) components, and it directly opposes the action of MLL-family histone methyltransferases. By removing H3K4 methylation at promoter regions, KDM5D silences genes involved in cell cycle progression and differentiation.
In the MCF-7 breast cancer context, knockout of KDM5D is predicted to elevate H3K4me2/3 levels at target gene promoters, leading to derepression of otherwise silenced loci. This epigenetic rewiring can perturb estrogen receptor-driven transcriptional programs and influence cell proliferation and hormone responsiveness. Consequently, this knockout system provides a valuable platform to dissect how KDM5D-mediated H3K4 demethylation impacts breast cancer cell phenotypes, including those associated with endocrine therapy resistance.
These polyclonal KDM5D knockout cells are applicable to a broad range of epigenetic and cancer biology investigations. Typical experimental approaches include ChIP-qPCR or ChIP-seq to map genome-wide changes in H3K4 methylation, RNA-seq to identify genes dysregulated upon KDM5D loss, and functional assays such as cell proliferation and hormone-response studies. Validation can be performed via Western blot or immunofluorescence for H3K4me2/3. For further technical details or to inquire about custom gene editing services, please contact Ascent Research.
