The KDM5B Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of TE1 human esophageal squamous cell carcinoma cells with targeted disruption of the KDM5B gene. This model provides a heterogeneous pool of loss-of-function alleles for functional studies without clonal selection, enabling robust analysis of KDM5B-dependent phenotypes in a cancer context.
The TE1 cell line is an epithelial model of human esophageal squamous cell carcinoma, commonly employed for investigating tumorigenesis, drug responses, and molecular mechanisms of this malignancy. Its genetic characteristics make it a valuable host for knockout studies examining genes involved in esophageal cancer progression and treatment resistance.
KDM5B encodes a histone H3K4me2/me3 demethylase that acts as a transcriptional repressor, forming complexes with SIN3A, HDAC1/2, REST, and Polycomb repressive complex 2 (PRC2) components such as EZH2 to silence gene expression. Its activity is regulated by MYC, HIF1A, NOTCH1, WNT signaling, and miR-137, and it represses targets including CCND1, CDKN1A, CDH1, and HOX genes. Through these interactions, KDM5B controls cell proliferation, differentiation, stem cell self-renewal, and epithelial-mesenchymal transition, with dysregulation contributing to cancer.
In TE1 cells, KDM5B knockout disrupts the demethylase function underlying tumor aggressiveness and cancer stem cell maintenance. This model permits dissection of KDM5B’s roles in esophageal squamous cell carcinoma growth, EMT, and histone modification dynamics, as well as its crosstalk with MYC and Notch pathways. Epigenetic and phenotypic changes following knockout can be systematically assessed to elucidate its contribution to tumor biology.
Applications include functional genomics, epigenetic drug screening, and chromatin remodeling studies. The cells support standard assays such as Western blotting for histone marks and protein levels, RT-qPCR, ChIP-qPCR, immunofluorescence, and functional assays assessing proliferation, migration, and colony formation. For more information, contact Ascent Research.
