ITGB3BP Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, engineered to disrupt the ITGB3BP gene. This loss-of-function model enables the study of ITGB3BP-dependent processes in a physiologically relevant intestinal epithelial context. The polyclonal population, generated without single-cell cloning, preserves genetic diversity while providing a robust knockout background for functional assays.
HT29 cells are a widely used in vitro model of intestinal epithelium, originating from a human colorectal adenocarcinoma. They exhibit epithelial morphology and are extensively employed to investigate intestinal barrier integrity, mucin production, and colorectal cancer pathogenesis. This cell line retains key signaling pathways relevant to tumor biology, making it an appropriate host for dissecting the roles of cancer-associated genes.
ITGB3BP (integrin beta 3 binding protein) functions as a transcriptional coregulator that integrates signals from integrin receptors and nuclear receptors. It physically interacts with integrin beta 3 (ITGB3), estrogen receptor alpha (ESR1), and the androgen receptor (AR), and cooperates with coactivators such as NCOA1 and NCOA2. Downstream, ITGB3BP influences the expression of cell cycle and apoptosis regulators including CCND1, BCL2, BAX, and MYC. Through its participation in the ITGB3?CFAK?CSRC?CPI3K?CAKT and nuclear receptor pathways, ITGB3BP promotes cell cycle progression and survival. Its knockout disrupts integrin-mediated adhesion signaling and nuclear receptor coactivation, potentially impairing downstream effector cascades and leading to altered proliferation and apoptotic responses.
In HT29 colorectal cancer cells, disruption of ITGB3BP is expected to perturb the integrin beta 3?CFAK?CAKT signaling axis and attenuate nuclear receptor transcriptional programs, thereby modulating cell cycle dynamics and apoptosis sensitivity. This knockout model may exhibit reduced tumorigenic properties, reflecting the gene’s role in colorectal cancer progression. The HT29 background provides a relevant intestinal tumor microenvironment, enabling researchers to explore how ITGB3BP loss influences cancer cell behavior, including migration, invasion, and response to growth factors.
This polyclonal knockout cell population is suited for functional genomics studies, drug target validation, and mechanistic investigations of integrin and nuclear receptor signaling in colorectal cancer. Typical applications include apoptosis assays (annexin V staining), proliferation assays (MTT), migration and invasion assays, and immunoblotting or RT-qPCR to examine downstream targets such as CCND1 and BCL2. Co-immunoprecipitation and reporter assays can further dissect ITGB3BP interactions with ESR1 or AR. Researchers can employ these cells to screen therapeutics targeting the integrin?CFAK pathway or nuclear receptor modulators. For additional information or to request custom gene-edited models, please contact Ascent Research.
