CCDC93 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma cell line. This heterogeneous pool of genome-edited cells is designed to disrupt the CCDC93 gene, providing a versatile loss-of-function model. The polyclonal format reflects a spectrum of gene-editing events, avoiding clonal selection artifacts and enabling studies of diverse cellular responses within a relevant epithelial background.
HT29 cells are a widely used human intestinal epithelial model established from a primary colorectal adenocarcinoma. These cells retain key epithelial characteristics including polarity, differentiation capacity, and secretory functions, making them suitable for investigations of intestinal biology, protein trafficking, and signal transduction. Their colorectal cancer origin renders them particularly valuable for studying oncogenic processes, such as dysregulated endosomal recycling and aberrant copper homeostasis, that are often perturbed in tumorigenesis.
CCDC93 functions as a core component of the CCC (COMMD?CCCDC22?CCCDC93) complex, which localizes to endosomal membranes and governs the recycling of integral membrane proteins. This complex is activated by copper levels and endocytic signals, and it directly interacts with COMMD1?C10 family members and CCDC22. Through these interactions, the CCC complex controls the cell surface delivery and recycling of copper transporters ATP7A and ATP7B, critical regulators of intracellular copper homeostasis. In parallel, CCDC93 modulates NF-??B signaling by regulating the degradation of signaling intermediates, thereby linking copper metabolism to inflammatory pathway activation. Thus, CCDC93 serves as a key node integrating metal ion sensing with transcriptional control.
In the HT29 colorectal adenocarcinoma setting, depleting CCDC93 allows for dissection of CCC complex functions that are frequently altered in colorectal cancer. Copper imbalance and NF-??B hyperactivation are hallmarks of tumor progression, and the loss of CCDC93 disrupts endosomal protein sorting, potentially affecting copper efflux, cell proliferation, and survival pathways. This polyclonal knockout model provides a physiologically relevant system to examine how defective copper handling and altered signaling contribute to oncogenic phenotypes in intestinal epithelial cells.
This CCDC93 knockout cell product is suitable for a range of research applications, including copper homeostasis studies, endosomal trafficking analysis, colorectal cancer biology, and NF-??B pathway investigation. It supports diverse assays such as Western blotting and immunofluorescence for protein expression and localization; copper uptake and endocytosis assays to assess metal transport and membrane recycling; NF-??B reporter systems for transcriptional activity; and cell viability assays for functional readouts. The polyclonal population ensures a robust platform for probing heterogenous cellular responses. For further details or to order, please contact Ascent Research.
