CCNYL1 Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-mediated polyclonal knockout cell population in which the CCNYL1 gene has been disrupted in the A2780 human ovarian carcinoma cell line. This product provides a heterogeneous loss-of-function model suitable for investigating CCNYL1-dependent signaling and cellular functions without enrichment for a single clonal genotype.
The host cell line A2780 is an epithelial ovarian carcinoma model derived from an untreated endometrioid adenocarcinoma patient tumor. It is widely employed in ovarian cancer research for studying signal transduction, drug response, and metastatic mechanisms, making it a relevant background for exploring genes involved in Wnt-driven tumor progression.
CCNYL1 encodes a cyclin-like protein that forms functional complexes with cyclin-dependent kinases CDK14 (PFTK1) and CDK16 (PCTK1). Upon activation by non-canonical Wnt ligands such as WNT5A and WNT11 through Frizzled receptors and Dishevelled (DVL), CCNYL1-CDK complexes promote phosphorylation events that activate the small GTPases RAC1 and RHOA, leading to downstream JNK and AP-1 signaling. This molecular cascade regulates actin cytoskeleton reorganization and cell migration, while also contributing to cell cycle progression. Key interaction partners include DVL and RAC1, positioning CCNYL1 at the intersection of Wnt/planar cell polarity and cell cycle control.
In the A2780 ovarian cancer context, CCNYL1 knockout is particularly valuable for dissecting contributions of non-canonical Wnt signaling to tumor cell motility and invasion. Aberrant Wnt pathway activity is frequently associated with ovarian cancer metastasis, and loss of CCNYL1 allows researchers to examine its specific role in actin dynamics, Rho GTPase-driven migration, and potential cross-talk with other oncogenic networks within an epithelial adenocarcinoma background.
This polyclonal knockout population supports a broad array of research applications, including functional analyses of CCNYL1 in cell migration via wound healing and transwell invasion assays, assessment of RAC1 and RHOA activity using Rho GTPase activation assays, and phospho-JNK evaluation by Western blotting. It is also amenable to immunofluorescence staining for actin cytoskeleton visualization, cell cycle profiling, and drug target validation studies aimed at ovarian cancer therapeutics. For further details, please contact Ascent Research.
