The CCDC9 knockout HT29 polyclonal cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma line. This product provides a heterogeneous pool of cells carrying targeted disruption of the CCDC9 gene, enabling loss-of-function studies without clonal selection. The polyclonal format captures a range of editing outcomes, offering a robust model for evaluating gene function in a disease-relevant epithelial context.
The HT29 cell line originates from a human colon adenocarcinoma and exhibits characteristic epithelial morphology. Widely utilized in cancer biology and intestinal epithelial research, HT29 cells serve as a well-characterized model for studying colorectal cancer pathology, including proliferation, differentiation, and therapeutic responses. Their established culture conditions and reproducible behavior make them an ideal host for gene knockout experiments.
CCDC9 encodes a coiled-coil domain-containing protein hypothesized to function as a tumor suppressor by engaging the TP53 pathway. In response to cellular stress, CCDC9 is regulated by TP53 and DNA damage signals, likely involving ATM kinase activation. It interacts with TP53 and MDM2, and transcriptionally promotes expression of downstream targets such as CDKN1A (p21) and BAX. These effectors orchestrate cell cycle arrest and apoptosis, thereby maintaining genomic integrity. Disruption of CCDC9 abrogates this signaling axis, potentially leading to unchecked proliferation and enhanced cell survival.
In the context of HT29 colorectal adenocarcinoma cells, knockout of CCDC9 is anticipated to compromise the TP53-dependent tumor suppressor network, providing a powerful tool to dissect the molecular underpinnings of colorectal cancer progression. This model enables researchers to interrogate how loss of CCDC9 influences cell cycle checkpoints, DNA damage repair, and apoptotic thresholds in an epithelial tumor background. The polyclonal knockout population is particularly suited for studying phenotype heterogeneity and for screening compounds that may restore or bypass CCDC9 function.
Typical applications encompass functional genomic analyses of CCDC9 in colorectal cancer, drug screening for targeted therapies, and mechanistic investigations of p53-dependent apoptosis. Researchers can employ a panel of assays with these cells, including western blotting for TP53 and p21, RT-qPCR for CCDC9 and downstream targets, MTT proliferation assays, annexin V apoptosis assays, flow cytometric cell cycle analysis, and colony formation assays. This versatile resource supports both academic and pharmaceutical research directed at elucidating tumor suppressor pathways and developing novel anticancer strategies. For additional technical information or support, please contact Ascent Research.
