The CCDC71L Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product provides a loss-of-function model for the CCDC71L gene, which encodes an uncharacterized coiled-coil domain-containing protein predicted to participate in centrosome organization and cell cycle progression. The polyclonal knockout population enables robust investigation of CCDC71L function without the clonal selection limitations, offering a heterogeneous genetic background that more closely mimics natural tumor heterogeneity.
The HT29 cell line was originally established from a primary colorectal adenocarcinoma of a female patient. These cells exhibit an epithelial morphology and harbor wild-type p53 along with a well-characterized APC mutation, making them a classic model for intestinal epithelial differentiation and barrier function. Their genetic background provides a relevant platform for studying colorectal cancer biology, particularly in the context of centrosome and cell cycle dysregulation commonly observed in malignant progression.
CCDC71L encodes a coiled-coil domain-containing protein predicted to function in centrosome duplication and cell cycle regulation. Evidence suggests that CCDC71L acts downstream of cell cycle kinases such as CDKs and is regulated by mitotic regulators PLK1 and Aurora A. The protein interacts with centrosomal components including gamma-tubulin and centrosomin, contributing to centrosome assembly and mitotic spindle formation. CRISPR/Cas9-mediated disruption of CCDC71L is thus expected to impair these processes, potentially causing defects in cell cycle progression and mitotic fidelity.
In the HT29 colorectal cancer model, loss of CCDC71L offers a tool to examine the role of centrosome integrity in tumor cell behavior. APC-mutant colorectal cancers often exhibit chromosomal instability, and centrosome dysfunction can further destabilize the genome. CCDC71L knockout enables investigation of how centrosome-related defects affect proliferation, differentiation, and barrier function in intestinal epithelial cancer cells, potentially uncovering therapeutic targets.
This polyclonal knockout product is ideally suited for functional studies of CCDC71L in cancer cell biology, including centrosome and cell division research, as well as colorectal cancer modeling. Recommended assays include immunofluorescence staining for centrosomal markers (e.g., gamma-tubulin), cell cycle analysis by flow cytometry with propidium iodide, proliferation assays such as MTT or BrdU, migration and invasion assays using Transwell chambers, and western blotting for cell cycle proteins like CDK1 and PLK1. For further information or to place an order, please contact Ascent Research.
