GPC1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HT29 human colorectal adenocarcinoma cells with targeted disruption of the GPC1 gene. This heterogeneous knockout pool provides a genetically diverse loss-of-function model for studying collective effects of GPC1 ablation on signaling networks and cellular phenotypes, avoiding clonal artifacts inherent to single-cell-derived lines. It is designed for bulk population studies where functional attenuation of glypican-1 is assessed across the entire cell ensemble.
HT29 is a widely used human colorectal adenocarcinoma cell line derived from a 44-year-old female with colon cancer. These adherent epithelial cells exhibit mucin production and differentiation capacity, serving as a physiologically relevant model for intestinal epithelial biology and cancer research. HT29 cells are instrumental for studying colorectal tumorigenesis and cell signaling in the context of malignant progression.
GPC1 encodes a cell surface heparan sulfate proteoglycan that acts as a coreceptor for growth factors such as FGF2, HGF, and Wnt3a, facilitating ligand-receptor binding and activating downstream pathways. Through FGFR1/FRS2, it potentiates RAS/RAF/MEK/ERK signaling, and via MET/GAB1 it enhances PI3K/AKT activation. GPC1 also modulates Wnt/??-catenin signaling through Frizzled/LRP6 complexes and Hedgehog signaling via Patched1. Overexpression results in increased ERK1/2 and AKT phosphorylation, ??-catenin nuclear translocation, and upregulation of cyclin D1 and VEGF, driving proliferation, migration, and angiogenesis.
In HT29 colorectal cancer cells, GPC1 sustains malignant phenotypes through growth factor signaling loops. Disruption of GPC1 in this polyclonal knockout enables dissection of its role in proliferation, survival, invasion, and tumor microenvironment interactions. Given the prevalence of dysregulated Wnt, Hedgehog, and FGF signaling in colorectal cancer, this model is valuable for analyzing how loss of a shared coreceptor affects these pathways and for evaluating GPC1 as a therapeutic target.
These cells are applicable for colorectal cancer signaling studies, drug target validation, and GPC1-targeted therapy screening. Typical assays include Western blotting, RT-qPCR, RNA-seq, MTS/CCK-8 proliferation, Transwell migration/invasion, phospho-ERK/AKT ELISA, flow cytometry, co-immunoprecipitation, Wnt reporter, and apoptosis assays. This polyclonal knockout platform advances GPC1 biology research in colorectal cancer. For more information or custom projects, contact Ascent Research.
