CCR9 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HCT 116 human colorectal carcinoma cells. This product comprises a heterogeneous pool of cells with targeted disruption of the CCR9 gene, achieved through CRISPR/Cas9-mediated gene editing, providing a loss-of-function model for functional studies.
HCT 116 is an epithelial colorectal carcinoma cell line harboring an MLH1 mismatch repair mutation, resulting in microsatellite instability. This well-characterized model is widely utilized in colorectal cancer research to study tumor cell biology, drug responses, and DNA repair mechanisms, and its adherent growth facilitates diverse assay formats.
CCR9 is a G protein-coupled receptor that selectively binds the chemokine CCL25. Ligand engagement activates G??i proteins, initiating signaling through PI3K-AKT and MAPK/ERK cascades. Key downstream effectors include AKT1 and MAPK1/MAPK3, which regulate cell survival and proliferation, and RAC1, which drives actin remodeling. Integrin ITGB1 and laminin LAMA4 act as effectors that facilitate cell adhesion and migration in response to CCR9 stimulation. The receptor is regulated by upstream signals from CCL25, TNFSF14, and Notch, and interacts with ARRB1/ARRB2 for desensitization and with JAK2 for noncanonical signaling. This molecular network integrates into chemokine signaling, PI3K-Akt, MAPK, and focal adhesion pathways.
In HCT 116 colorectal carcinoma cells, CCR9 expression has been associated with enhanced invasive potential and metastasis. The mismatch repair?Cdeficient background of HCT 116 provides a clinically relevant context, as MLH1 mutations are common in colorectal cancer. Knocking out CCR9 in this polyclonal pool allows investigation of the receptor??s role in tumor-intrinsic processes such as proliferation, apoptosis, and migration, without the confounding effects of clonal selection. The model is particularly suited to dissecting how CCR9 modulates signaling pathways that intersect with oncogenic drivers.
Typical applications include Transwell migration assays to measure CCL25-directed chemotaxis, phospho-AKT and phospho-ERK analysis via western blotting or flow cytometry, and proliferation or apoptosis assays. The cells can be used for RT-qPCR validation of downstream targets and for screening small-molecule CCR9 antagonists. Co-culture with immune cells enables studies of tumor microenvironment interactions. For technical assistance or customization inquiries, please contact Ascent Research.
