The CCNYL1 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited pooled population of human 786-O cells, each carrying distinct indel mutations that disrupt the CCNYL1 gene. This polyclonal knockout product provides a loss-of-function model for studying CCNYL1 in a renal cell carcinoma context.
The 786-O cell line is derived from a female patient with clear cell renal cell carcinoma (ccRCC) and harbors a VHL tumor suppressor mutation, resulting in constitutive HIF activation and tumorigenic properties. This well-characterized line serves as a relevant model for ccRCC pathophysiology and oncogenic signaling.
CCNYL1 encodes a cyclin-like regulatory subunit that interacts with cyclin-dependent kinases, primarily CDK14 and CDK16. Upstream growth factors such as EGF and FGF, acting through their receptors, promote CCNYL1-mediated CDK activation. These complexes phosphorylate RB1, releasing E2F transcription factors that transactivate genes encoding Cyclin D and Cyclin E, thereby promoting the G1-to-S phase transition.
Knockout of CCNYL1 in 786-O cells disrupts this cascade, impairing RB1 phosphorylation and E2F activity, leading to reduced proliferation and cell cycle arrest. This phenotype highlights the gene’s role in sustaining cell division in VHL-mutant ccRCC and provides a model for exploring cell cycle dysregulation.
Researchers can employ these cells in diverse assays: western blotting and RT-qPCR for expression analysis; flow cytometry for cell cycle profiling; BrdU, MTT, and colony formation assays for proliferation. They are suitable for inhibitor screening targeting cell cycle kinases and for validating CCNYL1 as a therapeutic target. For inquiries, contact Ascent Research.
