CC2D1A Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-mediated loss-of-function model in which the CC2D1A gene has been disrupted in the human colorectal adenocarcinoma HT29 cell line. This product consists of a polyclonal population of edited cells, providing a heterogeneous knockout background suitable for studying gene function in bulk cellular contexts. The targeted disruption of CC2D1A impairs its transcriptional repressor function, enabling researchers to investigate the downstream molecular consequences in a well-established intestinal epithelial model.
The HT29 parental cell line is derived from a human colorectal adenocarcinoma and exhibits epithelial morphology with adherent growth. Widely employed as an intestinal epithelial model, HT29 cells retain key signaling pathways relevant to colon cancer biology, including NF-??B, Wnt/??-catenin, and Notch. This background makes the CC2D1A knockout particularly relevant for exploring gene regulation in colorectal tumorigenesis and intestinal homeostasis.
CC2D1A encodes a transcriptional repressor that silences gene promoters by recruiting histone deacetylases, particularly HDAC1, thereby modulating pathways critical for cell proliferation and survival. Its downstream targets include HTR1A (serotonin receptor 1A) and DRD2 (dopamine receptor D2), linking CC2D1A to serotonin receptor signaling, as well as RELA of the NF-??B pathway and the anti-apoptotic factor BCL2. CC2D1A also interacts with RELA, HDAC1, and forms CC2D1A homodimers, integrating signals from upstream NF-??B and neuronal activity pathways. Through these interactions, CC2D1A coordinates transcriptional repression across multiple signaling networks, including Notch and Wnt/??-catenin, as evidenced by its influence on NOTCH1, CTNNB1, and TCF7L2.
In the HT29 colorectal cancer context, CC2D1A knockout is expected to derepress its target genes, potentially upregulating HTR1A, DRD2, and pro-survival factors like BCL2, while altering NF-??B dynamics. This dysregulation may drive changes in proliferation, apoptosis resistance, and motility, mirroring processes in colorectal cancer progression. Moreover, because CC2D1A is implicated in neurodevelopmental disorders, this intestinal epithelial model offers a unique tool to examine ectopic expression and signaling of neuronal genes in a cancer setting, bridging cancer biology and neurobiology.
This polyclonal knockout cell population is ideally suited for functional genomics studies, drug target screening (e.g., against serotonin receptor or NF-??B pathway modulators), and neurodevelopmental disorder modeling in intestinal cells. Researchers can employ a range of assays including RT-qPCR for HTR1A, western blot analysis of NF-??B/RELA and HDAC1, MTT and colony formation assays for proliferation, Annexin V apoptosis assays, and migration/invasion experiments, supplemented by RNA-seq transcriptomic profiling. For further details or to discuss custom applications, please contact Ascent Research.
