The BRD2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human HT29 colorectal adenocarcinoma cells, featuring targeted disruption of the BRD2 gene. BRD2 encodes a bromodomain-containing member of the BET family that reads acetylated histones and regulates transcription. The polyclonal format preserves heterogeneous editing events, avoiding clonal artifacts and enabling robust loss-of-function analysis.
HT29 cells are an adherent epithelial line derived from a colon adenocarcinoma, characterized by mutant p53 and widely used as a model for intestinal epithelial function and colorectal cancer. Their tumorigenic properties and well-mapped signaling pathways make them a suitable host for studying epigenetic regulators like BRD2 in a disease-relevant context.
BRD2 binds acetylated histone H4 via its bromodomains, recruiting co-activators such as p300/CBP and MED1 to promote transcription of proliferation and survival genes. It is activated by upstream ERK kinases and transcription factors E2F and MYC, and drives expression of downstream targets including MYC, CCND1 (cyclin D1), BCL2, and CDK4. BRD2 functions within MAPK/ERK, NF-??B, and JAK/STAT pathways, interacting with BRD4 and other chromatin modifiers to sustain oncogenic signaling.
In p53-mutant HT29 cells, BRD2 knockout disrupts BET-dependent transcriptional activation, reducing oncogene expression and impairing cell cycle progression and survival. This model enables dissection of BRD2-specific roles distinct from BRD4, and evaluation of colorectal cancer addiction to BET bromodomain activity.
Applications include western blotting for BRD2 and downstream targets, RT-qPCR and RNA-seq for transcriptomic analysis, ChIP-qPCR for histone acetylation, and functional assays such as MTT/XTT proliferation, caspase-3/7 apoptosis, and transwell migration/invasion. The cells are also suited for BET inhibitor (e.g., JQ1) sensitivity testing. For further information, contact Ascent Research.
