The CCNY Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from A-549 human lung adenocarcinoma cells, designed for functional studies of cyclin Y (CCNY). This product provides a heterogeneous pool of cells carrying CRISPR/Cas9-mediated disruptions in the CCNY gene, enabling loss-of-function analysis without clonal selection. The polyclonal format preserves native genetic diversity while abolishing CCNY expression across the population, making it suitable for pooled screening and robust phenotypic assays.
The A-549 host cell line originates from the lung adenocarcinoma of a 58-year-old male and serves as a well-characterized in vitro model of alveolar type II epithelial cells. These adherent epithelial cells retain key features of lung adenocarcinoma, including active Wnt signaling and unregulated proliferation, providing a clinically relevant background for studying the intersection of cell cycle control and oncogenic pathways. The cells are widely employed in cancer biology, drug discovery, and signaling research.
CCNY encodes a cyclin that partners with the cyclin-dependent kinase CDK14 (PFTK1) to phosphorylate the Wnt co-receptor LRP6, thereby potentiating Wnt/??-catenin signaling. This interaction promotes ??-catenin stabilization and transcriptional activation of TCF/LEF target genes, including cyclin B and CDK1, which facilitate the G2/M transition. CCNY activity is modulated by upstream Wnt ligands such as Wnt3a and serum growth factors, and integrates signals through the Dishevelled?CAxin?CGSK3?? axis, ultimately driving cell cycle progression and proliferation.
In the A-549 lung adenocarcinoma context, CCNY knockout disrupts LRP6 phosphorylation and attenuates ??-catenin?Cdriven transcription, providing a defined system to dissect the role of cyclin Y in tumor cell proliferation and invasive behavior. This model enables researchers to investigate how CCNY-mediated regulation of the G2/M checkpoint affects cancer growth, and to explore its contribution to Wnt-dependent invasion and metastasis, offering insights into potential therapeutic vulnerabilities in lung adenocarcinoma.
The CCNY Knockout A-549 Polyclonal Cells are suited for a broad range of experimental applications, including western blotting for CCNY, phospho-LRP6, ??-catenin, and cell cycle markers; RT-qPCR analysis of Wnt target genes; flow cytometric cell cycle profiling; ??-catenin/TCF reporter assays; and proliferation or migration/invasion assays. Co-immunoprecipitation can validate the CDK14?CCCNY interaction. This polyclonal population is ideal for genetic screens, drug target validation, and mechanistic studies of Wnt-regulated cell cycle control. For further details, please contact Ascent Research.
