The ING2 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product consists of a heterogeneous pool of cells harboring CRISPR/Cas9-mediated gene disruption of ING2, the inhibitor of growth family member 2 tumor suppressor. The polyclonal format preserves population-level functional diversity while providing a robust loss-of-function model for studying ING2-dependent processes.
HT29 cells are a well-established epithelial cell line originally isolated in 1964 from a primary colorectal adenocarcinoma. They exhibit an epithelial morphology and retain the capacity to differentiate into intestinal-like cells under appropriate culture conditions, making them a valuable model for intestinal epithelial biology. Widely employed in cancer research, HT29 cells are particularly useful for investigating colorectal tumorigenesis, epithelial differentiation, and drug response mechanisms.
ING2 is a stoichiometric component of histone acetyltransferase (HAT) and histone deacetylase (HDAC) complexes, linking DNA damage signals to chromatin remodeling and p53-dependent transcription. It directly interacts with p53, p300/CBP, HDAC1, HDAC2, SAP30, and Sin3A to regulate p53 acetylation and transcriptional activity. Downstream, ING2-mediated p53 activation promotes expression of p21/CDKN1A for cell cycle arrest and BAX for apoptosis. Loss of ING2 impairs these responses, fostering unchecked proliferation and survival. ING2 also participates in TGF-beta signaling, influencing NF-kB and TGF-beta target gene transcription, thereby integrating multiple tumor-suppressive networks.
In HT29 colorectal adenocarcinoma cells, ING2 knockout provides a physiologically relevant system to study tumor suppression mechanisms. HT29 cells possess an epithelial phenotype and can undergo differentiation, recapitulating aspects of intestinal epithelium. Ablation of ING2 disrupts p53-mediated apoptosis and cell cycle arrest, mirroring events that drive colorectal cancer progression. This polyclonal knockout model captures diverse editing events, offering a robust tool for dissecting ING2-dependent pathways in a cancer-relevant context without the constraints of clonal selection.
This ING2 knockout polyclonal population is suitable for a range of assays, including western blotting and RT-qPCR to verify ING2 loss and downstream effects on p21 and BAX; cell viability and apoptosis assays (e.g., Annexin V staining) following genotoxic challenge; flow cytometric cell cycle analysis; migration and invasion assays; colony formation; ChIP-qPCR for p53-chromatin interactions; and transcriptomic analysis via RNA-seq. It also supports drug sensitivity profiling to study chemoresistance in colorectal cancer. For further technical details or custom inquiries, please contact Ascent Research.
