The KDM5C Knockout TE1 Polyclonal Cells product provides a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 esophageal squamous cell carcinoma line, specifically engineered to disrupt the KDM5C gene. This polyclonal format maintains cellular diversity while effectively targeting KDM5C function, enabling robust loss-of-function analysis without the need for single-cell cloning. The approach leverages CRISPR/Cas9-mediated gene disruption to generate a heterogeneous pool of cells, facilitating studies that do not require clonal homogeneity but benefit from a targeted knockout background.
The parental TE1 cell line is isolated from a human esophageal squamous cell carcinoma and serves as a widely utilized epithelial cancer model. TE1 cells recapitulate key features of the tumor of origin, including aberrant growth signaling and invasive potential, and are extensively employed in research on esophageal tumorigenesis, metastasis, and chemoresistance. This context renders TE1 an ideal host for exploring the role of epigenetic regulators like KDM5C in esophageal malignancy, where histone modification dynamics are often perturbed.
KDM5C encodes a specific histone H3K4 demethylase that catalyzes the removal of methyl groups from mono-, di-, and trimethylated lysine 4 of histone H3, a mark associated with active gene promoters. This activity is transcriptionally controlled by REST and microRNAs, positioning KDM5C downstream of these regulatory inputs. KDM5C, in turn, modulates the expression of critical downstream targets, including HOX genes, tumor suppressors, and oncogenes, thereby influencing cell fate decisions. It physically interacts with HDACs and RB proteins, integrating into chromatin-modifying complexes that also involve H3K4 methyltransferases, Polycomb group proteins, and trithorax group proteins. Through this coordinated network, KDM5C helps maintain proper H3K4 methylation dynamics at genomic loci essential for development and tumor suppression.
Disruption of KDM5C in TE1 esophageal carcinoma cells is expected to markedly alter the H3K4 methylation landscape, leading to the derepression of developmentally regulated genes and dysregulation of transcriptional programs governing cell proliferation, apoptosis, and differentiation. This model recapitulates epigenetic aberrations frequently observed in esophageal squamous cell carcinoma, where histone modification imbalances contribute to disease progression. Importantly, loss-of-function mutations in KDM5C cause X-linked intellectual disability (Claes-Jensen syndrome) and have been associated with renal cell carcinoma, underscoring the gene??s significance in both neurodevelopmental and oncological contexts. The KDM5C knockout TE1 polyclonal cells therefore offer a versatile platform for dissecting the chromatin-mediated mechanisms underlying these diverse pathologies.
Applications for this polyclonal knockout model include chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) to assess global and locus-specific H3K4 methylation states (me3/me2/me1), RNA sequencing for transcriptome-wide expression profiling, and functional assays such as MTT or CCK-8 cell proliferation assays and transwell migration/invasion analyses. Researchers can employ these cells to study epigenetic regulation in esophageal cancer, screen for epigenetic drugs, or investigate the interplay between KDM5C and its molecular partners. For additional product details or to discuss custom requirements, please contact Ascent Research.
