The CCDC127 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, engineered for loss-of-function studies of the CCDC127 gene. This genetically disrupted polyclonal pool offers a versatile tool for investigating centrosome biology and genomic stability mechanisms without the constraints of single-cell clone selection. The heterogeneous knockout population enables robust assessment of CCDC127 function in a cellular context that retains the intrinsic variability of a polyclonal background.
The parental HT29 cell line is a widely utilized intestinal epithelial model originally isolated from the primary colorectal adenocarcinoma of a 44-year-old female patient. These adherent epithelial cells are characterized by their ability to differentiate under appropriate conditions, making them a valuable system for studying colorectal cancer progression, intestinal cell differentiation, and signaling pathway dysregulation. Their well-documented growth properties and responsiveness to various stimuli provide a reliable platform for functional genomics experiments.
CCDC127 encodes a coiled-coil domain-containing protein that localizes to the centrosome and is implicated in the regulation of centrosome duplication and mitotic progression. The protein interacts with key centrosomal components including gamma-tubulin, CEP135, and pericentrin, and is functionally linked to the mitotic kinase PLK1. CCDC127 operates downstream of CDK1-cyclin B and E2F transcription factors, and its activity influences the spindle assembly checkpoint, p53-mediated cell cycle arrest, and apoptotic pathways. Representative pathway components such as PLK4, STIL, SAS6, CPAP, and CDK2 are integral to the centrosome duplication machinery in which CCDC127 participates.
In the colorectal adenocarcinoma context of HT29 cells, disruption of CCDC127 leads to aberrant centrosome homeostasis, increasing the likelihood of mitotic errors, chromosome missegregation, and genomic instability. This perturbation can alter cell proliferation dynamics and may sensitize cells to stress responses, providing a relevant model to dissect how centrosomal defects contribute to tumorigenesis and cancer cell survival. The polyclonal nature of the knockout population captures a spectrum of gene disruption effects, reflecting the heterogeneity often observed in tumor biology.
These polyclonal knockout cells are well-suited for a range of experimental applications, including immunofluorescence-based assessment of centrosome integrity, Western blotting for centrosomal and cell cycle markers, and flow cytometric cell cycle profiling. They facilitate proliferation assays (MTT or BrdU), apoptosis detection via Annexin V staining, and migration and invasion assays using Transwell systems. This model is particularly valuable for chemical or genetic screens aimed at identifying regulators of mitotic fidelity and genome stability. For further information or to discuss custom applications, please contact Ascent Research.
