The CCDC82 Knockout 786-O Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt expression of the coiled-coil domain-containing protein CCDC82 in the human 786-O renal cell adenocarcinoma background. This gene-edited pool is generated via CRISPR/Cas9-mediated gene disruption, producing a heterogeneous loss-of-function model that facilitates robust functional studies without the bottleneck of clonal selection. The polyclonal format ensures representation of diverse editing events across the cell population, making it a powerful resource for investigating gene function in a physiologically relevant context.
The 786-O host cell line is a VHL-mutant clear cell renal cell carcinoma (ccRCC) line derived from a primary tumor of a patient with renal adenocarcinoma. As a cancerous epithelial cell model, 786-O cells exhibit characteristic dysregulated hypoxia-inducible factor (HIF) signaling due to biallelic VHL inactivation, which drives aberrant cell growth, migration, and metastatic potential. This genetic background provides a clinically pertinent platform for studying molecular mechanisms underlying renal cell carcinoma progression and for evaluating novel therapeutic targets.
CCDC82 encodes a coiled-coil domain-containing protein that is implicated in the regulation of cell proliferation and differentiation. Although its direct upstream regulators, downstream effectors, and interacting partners remain poorly characterized, structural predictions suggest it may form homo- or hetero-oligomeric complexes through its coiled-coil motifs, potentially engaging components of the cell cycle machinery. It is thought to act within signaling networks that modulate cell cycle progression, possibly interacting with or influencing the activity of key cell cycle regulators such as cyclins, cyclin-dependent kinases, or their inhibitors. Disruption of CCDC82 in this model permits dissection of its mechanistic contributions to these fundamental cellular processes.
In the context of VHL-mutant 786-O cells, knockout of CCDC82 allows researchers to assess the functional consequences of its loss on renal cancer cell proliferation, differentiation, and survival. This model is particularly valuable for exploring how CCDC82 may interface with oncogenic pathways driven by HIF stabilization and for determining its role in maintaining malignant phenotypes. The polyclonal knockout population captures the spectrum of genetic perturbations, enabling studies that are more representative of therapeutic target inhibition in a heterogeneous tumor environment.
Typical research applications include investigation of CCDC82 function in renal cell carcinoma, validation of CCDC82 as a potential drug target, and functional genomics screening to uncover synthetic lethal interactions. Researchers can employ a range of downstream assays such as western blotting and RT-qPCR to confirm target disruption, cell proliferation and cell cycle analyses to assess growth phenotypes, migration and invasion assays to evaluate metastatic behavior, and apoptosis assays to study programmed cell death. Transcriptomic profiling via RNA-seq can further elucidate pathway alterations. For further details, please contact Ascent Research.
