The ANKRD10 Knockout HT29 Polyclonal Cells represent a polyclonal population of HT29 human colorectal adenocarcinoma cells engineered via CRISPR/Cas9-mediated disruption of the ANKRD10 gene. This loss-of-function model enables systematic investigation of ANKRD10 function in a well-characterized epithelial cancer background. The polyclonal format preserves the genetic heterogeneity inherent to a population of edited cells, facilitating robust functional studies without clonal selection bias. This product is intended for researchers studying the molecular underpinnings of colorectal cancer and related malignancies.
HT29 cells are derived from a primary human colorectal adenocarcinoma and are widely employed as a model system for colon cancer biology, intestinal epithelial physiology, and preclinical drug evaluation. These cells retain characteristics of intestinal epithelial cells, including the capacity to differentiate and form polarized monolayers, making them particularly suitable for investigating processes such as proliferation, apoptosis, and migration in a cancer-relevant context. The HT29 background provides a clinically pertinent platform for dissecting the contribution of individual genes to tumorigenesis and therapy response.
ANKRD10 encodes a protein characterized by ankyrin repeat domains, which are known to mediate protein-protein interactions. However, the specific interacting partners, upstream regulators, and downstream effectors of ANKRD10 remain uncharacterized. Current bioinformatic predictions and limited functional data suggest a potential involvement in cell cycle regulation and apoptosis, consistent with its putative role in cancer development. The disruption of ANKRD10 in HT29 cells allows for the empirical assessment of these predictions, providing a clean genetic background to identify phenotypic consequences and interrogate associated signaling pathways.
The knockout of ANKRD10 in the HT29 colorectal adenocarcinoma model is particularly relevant given the reported associations of ANKRD10 dysregulation with colorectal, gastric, and hepatocellular carcinomas. By ablating ANKRD10 expression in this intestinal cancer cell line, researchers can directly evaluate its contribution to oncogenic phenotypes such as uncontrolled proliferation, resistance to apoptosis, and enhanced migratory capacity. This model thus serves as a critical tool for validating ANKRD10 as a potential therapeutic target and for unraveling its role in gastrointestinal and hepatic cancers.
This product is suitable for a broad range of applications in functional genomics and cancer biology, including validation of ANKRD10 as a drug target, protein interaction screens, and mechanistic studies of cancer cell behavior. Representative assays compatible with these polyclonal knockout cells include Western blotting and RT-qPCR for confirming gene disruption and quantifying expression changes, MTT or CCK-8 assays for proliferation, Annexin V staining for apoptosis, flow cytometry for cell cycle analysis, and Transwell assays for migration and invasion. For additional information or customized support, please contact Ascent Research.
