The CCNY Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the CCNY gene in HeLa cells. This loss-of-function model enables systematic investigation of Cyclin Y functions in cell cycle regulation, Wnt signaling, and actin cytoskeletal dynamics within a well-characterized cervical adenocarcinoma background. The polyclonal format provides a heterogeneous knockout pool, minimizing clonal selection bias while capturing diverse editing outcomes for population-level analyses.
HeLa cells, derived from HPV18-positive cervical adenocarcinoma, exhibit functional inactivation of p53 and Rb tumor suppressors, leading to deregulated cell cycle checkpoints and enhanced proliferation. This genetic context is directly relevant to cervical cancer research, offering a reproducible epithelial model with established growth kinetics for studying oncogenic signaling and therapeutic responses.
Cyclin Y (CCNY) forms active complexes with CDK14 to drive G2/M transition. The CCNY-CDK14 complex phosphorylates the Wnt co-receptor LRP6, enhancing Wnt/??-catenin signaling downstream of Wnt3a. Additionally, it modulates actin polymerization through the RhoA-ROCK-LIMK-cofilin cascade, linking cell cycle progression to cytoskeletal reorganization. CCNY expression is transcriptionally regulated by E2F1, and it interacts with 14-3-3 proteins and actin filaments. Key pathway members include CCNY, CDK14, LRP6, DVL, ??-catenin, RhoA, ROCK, LIMK, and cofilin.
In the HeLa setting, HPV-driven p53/Rb inactivation accentuates the dependence on cyclin-CDK and Wnt signaling for unchecked proliferation and motility. CCNY disruption allows dissection of how Cyclin Y influences G2/M progression, LRP6 phosphorylation, Wnt target gene expression, and actin-mediated migration. This model supports mechanistic and pharmacological studies on cervical adenocarcinoma proliferation, invasion, and cytoskeletal dynamics, with the polyclonal population reflecting heterogeneous cellular responses.
Typical applications include western blotting to verify Cyclin Y knockout and phospho-LRP6 changes, flow cytometry for cell cycle profiling, and RT-qPCR for Wnt target genes such as AXIN2. Migration and invasion assays, paired with fluorescent actin staining, quantify motility and cytoskeletal alterations. The cells are well-suited for drug sensitivity screening against CDK or Wnt pathway inhibitors. For technical specifications and ordering information, please contact Ascent Research.
