The CCDC102A Knockout 786-O Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CCDC102A gene in a human clear cell renal cell carcinoma (ccRCC) background. Derived from the 786-O cell line, this product delivers a heterogeneous pool of edited cells, enabling pooled functional screening and population-level analyses without clonal selection bias. The polyclonal format captures a spectrum of gene-disruption outcomes, making it suitable for experiments that benefit from a diverse knockout population rather than a single clonal isolate.
The 786-O host cell line is a widely used model of ccRCC, originating from the proximal tubule epithelium. These cells harbor a homozygous VHL gene deletion or frameshift mutation, resulting in constitutive stabilization of hypoxia-inducible factors HIF-1?? and HIF-2?? under normoxic conditions. Consequent persistent HIF transcriptional activity drives angiogenesis, metabolic rewiring, and oncogenic signaling, faithfully recapitulating key features of ccRCC tumor biology.
CCDC102A encodes a coiled-coil domain-containing protein with a putative role in centrosomal scaffolding and cytoskeletal organization. Functional data implicate it in centrosome duplication and cell cycle regulation, and it is believed to interact with centrosomal proteins such as CEP family members and microtubule-associated proteins. Representative pathway components that may interface with CCDC102A include ??-tubulin, pericentrin, CEP164, and the transcription factor HIF-1??, which is a candidate upstream regulator in the VHL-deficient ccRCC context. Upstream drivers and downstream effectors remain to be fully characterized.
In the 786-O background, CCDC102A knockout is expected to disrupt a centrosomal scaffold essential for mitotic spindle formation, impairing cell cycle progression and potentially generating genomic instability. This defect likely synergizes with the constitutively active HIF signaling axis, amplifying oncogenic phenotypes such as proliferation and migration. The model thus enables dissection of how centrosomal alterations intersect with HIF-driven transcriptional programs, offering a platform to probe crosstalk between these pathways in ccRCC.
Typical research applications span centrosome biology in cancer, functional genomics of ccRCC, and drug combination studies targeting HIF and centrosomal pathways. Researchers can validate knockout by Western blot, assess centrosome integrity via ??-tubulin immunofluorescence, quantify cell cycle distribution by flow cytometry, and evaluate functional consequences using wound healing migration assays and viability tests under hypoxia. This polyclonal knockout cell population serves as a versatile tool for both mechanistic and discovery-driven studies. For further technical information, please contact Ascent Research.
