The KDM5D Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous pool derived from the human esophageal squamous cell carcinoma (ESCC) cell line TE1, featuring disruption of the KDM5D gene. This loss-of-function model enables investigation of the Y chromosome-encoded histone demethylase KDM5D. The polyclonal format preserves the diversity of editing events, avoiding clonal artifacts and facilitating population-level functional analyses. The cells are provided as cryopreserved stocks and are suitable for a wide range of downstream applications in cancer epigenetics and drug discovery.
TE1 is an adherent epithelial ESCC cell line from a male patient, widely used for studying esophageal cancer. Its epithelial morphology and tumorigenic properties are preserved. The male origin is relevant for investigating Y chromosome gene functions and sex-specific cancer mechanisms. TE1 supports standard culture, transfection, and downstream assays.
KDM5D encodes a histone H3K4 demethylase that removes methyl marks from H3K4me1/2/3, regulating chromatin state and gene expression. It operates in complexes with HDAC1/2, NCOR1, REST, and components of the NuRD complex, and is modulated by upstream regulators including androgen receptor, p53, and miR-26a/b. By opposing MLL methyltransferases, KDM5D maintains H3K4 methylation balance. Its knockout leads to hypermethylation at promoters of targets like CDKN1A, CCND1, BAX, SNAI1, and ZEB1, disrupting cell cycle, apoptosis, and EMT transcription programs.
In the male TE1 background, KDM5D disruption enables the study of sex-dependent epigenetic mechanisms, as loss of this Y-linked demethylase causes H3K4 hypermethylation at target promoters. This alters expression of proliferation and apoptosis genes, offering insights into tumorigenicity and drug sensitivity. The polyclonal population reflects editing heterogeneity and avoids clonal artifacts.
Applications include RNA-seq, ChIP-qPCR for H3K4me3, flow cytometry for cell cycle/apoptosis, and proliferation assays. Suitable for screening demethylase or HDAC inhibitors and Boyden chamber migration/invasion studies. This model advances research on Y chromosome tumor biology and epigenetic therapy. For further assistance, please contact Ascent Research.
