The CCNYL1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma line, featuring targeted disruption of the CCNYL1 gene encoding a putative cyclin. This heterogeneous loss-of-function model enables unbiased interrogation of CCNYL1’s role in Wnt signaling and cell cycle control without monoclonal selection. The knockout is generated via CRISPR/Cas9-mediated genome editing, providing efficient gene disruption across the cell pool for robust functional studies in a well-characterized epithelial background.
HeLa cells, isolated in 1951 from a cervical adenocarcinoma, are HPV18-positive and highly aneuploid, with viral E6/E7 proteins inactivating TP53 and RB1. This genetic makeup makes HeLa a classic model for cancer biology, virology, and cell signaling studies. Their extensive characterization and reproducible growth confer significant advantages for CRISPR-based gene editing, establishing a reliable platform for dissecting CCNYL1 function in a disease-relevant context.
CCNYL1 encodes a cyclin-like regulatory subunit of CDK14 (PFTK1) and possibly CDK16. The CCNYL1?CCDK14 complex phosphorylates the Wnt co-receptor LRP6, triggering ??-catenin stabilization and TCF/LEF-mediated transcription, with TCF7L2 as a representative downstream factor. CCNYL1 is also implicated in non-canonical Wnt pathways through RAC1 and JNK. Its expression is driven by E2F transcription factors and mitogenic cues such as EGF and FGF, situating it at the nexus of growth factor signaling, cell cycle progression, and Wnt pathway modulation.
In HeLa cells, CCNYL1 knockout offers a unique system to study the intersection of HPV-mediated transformation and Wnt pathway regulation. Since TP53 and RB1 are disabled by viral oncoproteins, the model allows investigation of CCNYL1??s contribution to LRP6 phosphorylation, ??-catenin activity, and proliferation in a cervical cancer background. It provides a means to assess whether CCNYL1 represents a therapeutic target in cancers driven by dysregulated Wnt signaling.
This polyclonal knockout cell pool is amenable to diverse experiments: Western blotting and RT-qPCR for expression analysis, LRP6 phosphorylation and TOPFlash/FOPFlash reporter assays for Wnt pathway activity, co-immunoprecipitation with CDK14 for complex formation, and cell cycle flow cytometry or proliferation assays (MTT, BrdU) for phenotypic profiling. Apoptosis evaluation and drug sensitivity screens facilitate translational research. For additional information, please contact Ascent Research.
