BCL7A Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the human BCL7A gene. This product provides a heterogeneous pool of HT29-derived cells harboring loss-of-function mutations across the BCL7A locus, enabling functional studies without monoclonal selection. The polyclonal format preserves the genetic diversity of the knockout population, facilitating robust assessment of BCL7A-dependent phenotypes in an epithelial colorectal adenocarcinoma background. As an advanced model for chromatin remodeling and Wnt pathway research, this knockout cell product supports a broad range of molecular and pharmacological investigations.
Derived from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female, HT29 cells are a widely used adherent epithelial line with a microsatellite stable (MSS) genomic background. These cells harbor mutations in the APC, TP53, and PIK3CA genes while retaining wild-type KRAS and BRAF alleles, making them particularly valuable for studying Wnt-driven colorectal carcinogenesis. HT29 cells serve as a seminal model for intestinal epithelial biology, colorectal cancer progression, and therapeutic drug absorption, as well as for evaluating epithelial barrier function in vitro. Their well-characterized signaling landscape and robust growth characteristics make HT29 an ideal host for interrogating tumor-suppressor and chromatin-remodeling gene functions.
BCL7A encodes a core subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex, which orchestrates genome-wide nucleosome repositioning to regulate transcription. BCL7A directly interacts with the catalytic subunit SMARCA4 (BRG1) and scaffold subunits SMARCC1/2 (BAF155/170), and it bridges the BAF complex to ???catenin, thereby linking chromatin remodeling to Wnt-responsive gene expression. Mechanistically, BCL7A facilitates the transcriptional activation of key target genes including MYC, CCND1, and CDKN1A, while modulating apoptosis through BCL2 family members. Upstream regulators such as MYC and Wnt/???catenin signaling control BCL7A expression, establishing a regulatory feedback loop. Disruption of BCL7A compromises BAF complex integrity, altering chromatin accessibility at Wnt target loci and disrupting cell cycle and apoptotic balance??processes particularly relevant in APC-mutant colorectal cancer models.
In the HT29 context, constitutively active Wnt/??catenin signaling driven by APC truncation creates a sensitized background for examining BCL7A-dependent transcriptional control. Loss of BCL7A is expected to perturb the SWI/SNF complex??s ability to engage ???catenin and SMARCA4, leading to altered expression of downstream effectors such as MYC and CCND1 and potentially affecting tumor cell proliferation, apoptosis, and migration. This knockout model provides a powerful tool to dissect the intersection of chromatin remodeling and oncogenic Wnt signaling, offering insights into synthetic lethal interactions and novel therapeutic vulnerabilities in colorectal cancer. The HT29-BCL7A knockout system also enables investigation of epithelial barrier and drug absorption alterations driven by BCL7A loss.
Typical applications include chromatin immunoprecipitation sequencing (ChIP-seq) and RNA-seq to map genome-wide chromatin and transcriptional changes, RT?qPCR and Western blotting for target gene validation, and functional assays such as MTT proliferation, apoptosis flow cytometry, and wound healing migration. The TOPFlash Wnt reporter assay can quantify ???catenin/TCF4 transcriptional activity changes, and drug sensitivity screens enable testing of chemotherapeutic and targeted agents. This knockout product is ideally suited for mechanistic studies, synthetic lethality screens, and preclinical evaluation of therapeutics modulating SWI/SNF function. For additional information or custom inquiries, please contact Ascent Research.
