The BCL7C Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, providing a loss-of-function model for the BCL7C gene. This heterogeneous pool contains cells harboring targeted disruptions of the BCL7C locus, enabling functional studies without clonal selection. It is designed for investigations into BCL7C-dependent chromatin remodeling and tumor suppression.
HT29 cells are a widely used model of colorectal adenocarcinoma with epithelial morphology, extensively employed in cancer research and drug screening. They carry mutations in APC and TP53, resulting in constitutive activation of Wnt/??-catenin signaling, which makes them particularly relevant for studying this pathway. The cell line’s adherent growth and high transfectability facilitate a range of molecular and cellular assays.
BCL7C encodes a subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex that modulates transcription through nucleosome repositioning. In the Wnt pathway, BCL7C interacts with ??-catenin and TCF/LEF transcription factors, such as TCF7L2/TCF4, to regulate downstream targets including AXIN2, CCND1, MYC, BAX, and CDKN1A. It also associates with BAF core components SMARCA4, SMARCB1, and ARID1A. Upstream regulators include Wnt ligands like Wnt3a, the ??-catenin/TCF complex, and TP53. Through these interactions, BCL7C functions as a tumor suppressor by promoting pro-apoptotic and cell cycle inhibitory gene expression.
In HT29 cells, loss of BCL7C disrupts the balance between proliferation and apoptosis, mirroring its tumor suppressor role. This knockout model allows dissection of the interplay between BAF-mediated chromatin remodeling and Wnt-driven oncogenic transcription, providing a platform for studying the consequences of BCL7C inactivation. The polyclonal population captures the heterogeneity of gene disruption, reflecting the diverse mutations found in tumors.
Applications include functional analysis of BCL7C in Wnt/??-catenin signaling, chromatin occupancy studies via ChIP-qPCR, and transcriptomic profiling with RNA-seq. Knockout validation is performed by Sanger sequencing, Western blot, and RT-qPCR. Phenotypic assays such as MTT proliferation, Annexin V apoptosis, and TOP/FOP Flash reporter assays quantify cellular responses. Co-immunoprecipitation assesses interactions with ??-catenin or SMARCA4, and immunofluorescence reveals subcellular localization. For technical inquiries, contact Ascent Research.
