KIAA1191 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited population of HT29 colorectal adenocarcinoma cells featuring targeted disruption of the endogenous KIAA1191 gene (also known as C9orf10). As a polyclonal knockout pool, this model avoids the limitations of single-clone selection and is ideal for studying the collective consequences of KIAA1191 loss in an unselected cell population. The product is intended for functional characterization of this uncharacterized gene, which is predicted to be involved in cell cycle control and RNA metabolism.
HT29 cells are an established human colorectal adenocarcinoma line isolated from a primary tumor of a 44-year-old Caucasian female. These adherent epithelial cells form polarized monolayers and express markers of intestinal epithelium, making them a widely used model for colon cancer biology, mucosal barrier function, and drug permeability studies. The cell line carries mutations in APC and TP53, providing a genetically relevant context for investigating tumor cell proliferation, apoptosis, and therapeutic responses.
KIAA1191 is predicted to function downstream of the transcription factors E2F and p53, key regulators of cell cycle entry and apoptosis. Interactome analyses suggest physical association with RNA-binding proteins such as RBMX and HNRNPA1, implicating KIAA1191 in post-transcriptional regulation. Upon KIAA1191 knockout, downstream effectors may be dysregulated, including cyclin D1 (CCND1) and CDK4 for G1/S transition, as well as the BCL2/BAX axis controlling mitochondrial apoptosis, ultimately affecting caspase-3 (CASP3) activation. These interactions position KIAA1191 as a potential node integrating proliferation and survival signals.
In the HT29 colorectal cancer model, KIAA1191 loss-of-function allows direct interrogation of its contribution to malignant phenotypes. Given the gene’s predicted roles, knockout cells are expected to exhibit altered cell cycle progression, apoptosis sensitivity, or colony-forming ability, providing a platform to study how KIAA1191 interactions with mutated p53 and aberrant Wnt signaling influence tumor growth. This model is particularly valuable for identifying synthetic lethal interactions or differential drug sensitivities arising from KIAA1191 deficiency in the HT29 context.
Key applications include RT-qPCR and RNA-seq profiling of KIAA1191-dependent gene expression, cell viability measurements by MTT or CellTiter-Glo, apoptosis detection via Annexin V staining, and flow-cytometric cell cycle analysis. Long-term proliferation can be assessed through colony formation assays, and drug screening campaigns can exploit this model to identify compounds selectively active against KIAA1191-null cells. These polyclonal knockout cells are also suitable for high-throughput genetic or pharmacological screens. For technical assistance, protocol support, or custom gene-editing services, please contact Ascent Research.
