The CCDC127 Knockout 786-O Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the 786-O human renal cell carcinoma line, designed for functional studies of the CCDC127 centrosomal protein. This polyclonal format consists of a genetically diverse pool of cells with individual CCDC127 disruptions, capturing the biological variability of tumor cell populations and avoiding clonal selection artifacts. It provides a robust loss-of-function system for investigating CCDC127-dependent processes in a cancer-relevant setting.
The 786-O host cell line is a well-established model for clear cell renal cell carcinoma (ccRCC), originally isolated from a primary clear cell adenocarcinoma. These cells carry a characteristic loss-of-function mutation in the von Hippel-Lindau (VHL) tumor suppressor gene, which leads to stabilization of hypoxia-inducible factors (HIFs) and constitutive activation of downstream oncogenic pathways. This genetic background makes 786-O cells particularly valuable for exploring the interplay between centrosome biology and the molecular hallmarks of kidney cancer.
CCDC127 is a core structural component of the centriole cartwheel, physically interacting with PLK4, CEP152, CEP135, SASS6, STIL, and CENPJ to drive centriole biogenesis. Its transcription is activated by E2F transcription factors and FOXM1, and its function is coordinated with cell cycle kinases PLK1 and CDK1/cyclin B. CCDC127 acts upstream of the centriole duplication machinery by promoting the recruitment of SASS6 and CEP135 to the nascent procentriole. Loss of CCDC127 therefore prevents centriole duplication, disrupting centrosome organization and mitotic spindle formation.
Within the 786-O ccRCC context, CCDC127 knockout serves as a precise tool to examine how centrosomal dysfunction contributes to oncogenic processes. Loss of CCDC127 compromises centrosome fidelity, potentially exacerbating the genomic instability inherent in VHL-deficient cells and influencing tumor cell proliferation, survival, and invasive properties. This model therefore enables dissection of centrosome-related vulnerabilities that may be synthetically lethal with ccRCC driver mutations, opening avenues for targeted therapeutic strategies.
This product is ideal for immunofluorescence detection of centrosome proteins (e.g., CENPJ, CEP135), Western blotting, flow cytometry-based cell cycle profiling, and functional assays measuring proliferation, apoptosis, migration, and ciliogenesis. It also supports high-throughput drug screening to identify synthetic lethal interactions with CCDC127 deficiency in renal carcinoma cells. For more information, contact Ascent Research.
