The BCL7B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for investigating BCL7B function in colorectal adenocarcinoma. Derived from the HT29 epithelial cell line, this heterogeneous pool of cells carries targeted BCL7B gene disruptions, offering a robust loss-of-function model free of clonal selection bias. The knockout is mediated by CRISPR/Cas9, ensuring effective gene disruption. As a polyclonal population, it preserves genetic diversity, making it suitable for studies requiring averaged phenotypic responses and reducing single-cell cloning artifacts.
HT29 is a widely used human colorectal adenocarcinoma cell line established from a primary tumor of a 44-year-old female. These adherent epithelial cells express intestinal markers and are employed in cancer biology, intestinal epithelial studies, and drug absorption research. HT29 cells can differentiate and produce mucin under specific conditions, providing a physiologically relevant model for colorectal tumorigenesis and epithelial barrier function. Its well-characterized oncogenic background makes it an ideal host for examining tumor suppressor genes like BCL7B.
BCL7B encodes a subunit of the SWI/SNF chromatin remodeling complex, which regulates transcription through ATP-dependent nucleosome repositioning. As a tumor suppressor, BCL7B functions downstream of Wnt/??-catenin signaling, where it is transcriptionally activated by the ??-catenin/TCF/LEF complex. BCL7B interacts with core BAF components including SMARCA4, SMARCB1, and ARID1A, along with its paralogs BCL7A and BCL7C. This complex relays signals from Wnt ligands (e.g., WNT3A) and Frizzled/LRP receptors to control expression of downstream targets such as CCND1, MYC, and CDKN1A, thereby coordinating cell cycle progression and apoptosis.
In HT29 cells with constitutively active Wnt signaling, BCL7B knockout disrupts SWI/SNF-mediated transcriptional control, leading to dysregulation of cell cycle and apoptotic genes. This alteration is predicted to affect proliferation, differentiation, and tumorigenicity, creating a potent system for dissecting chromatin remodeling?Concogenic signaling crosstalk in colorectal cancer. By eliminating BCL7B function, researchers can evaluate the reliance of colorectal cancer cells on SWI/SNF complex integrity and investigate the mechanisms underlying BCL7B-mediated tumor suppression.
This polyclonal knockout population supports diverse applications in colorectal cancer and epigenetic research, including Wnt/??-catenin pathway studies, chromatin remodeling analysis, and tumor suppressor gene characterization. Representative assays: Western blotting and RT-qPCR for BCL7B and downstream targets (e.g., CCND1, MYC), RNA-seq for transcriptomics, ChIP-qPCR for chromatin occupancy, flow cytometry for cell cycle and apoptosis, co-immunoprecipitation for BAF complex interactions, TCF/LEF luciferase reporter assays, and MTT/CCK-8 proliferation assays. Drug sensitivity screening and migration/invasion studies are also feasible. For detailed technical support, please contact Ascent Research.
