The CCNYL1 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population for investigating cyclin Y-like protein 1 (CCNYL1) function in human gastric carcinoma. This heterogeneous HGC-27 cell pool harbors targeted disruptions at the CCNYL1 locus introduced by CRISPR/Cas9, enabling loss-of-function studies without clonal selection artifacts. The polyclonal format provides a robust genetic model for interrogating CCNYL1-dependent phenotypes and signaling networks in a well-characterized gastric cancer background.
HGC-27 is an epithelial tumor cell line derived from a lymph node metastasis of gastric carcinoma, widely employed in gastric cancer research. It mirrors key features of gastric adenocarcinoma, including aberrant Wnt/??-catenin pathway activation and disrupted cell cycle regulation. Retaining molecular hallmarks of metastatic disease, HGC-27 cells are ideal for studying tumor progression and drug resistance. CCNYL1 knockout in this background permits direct assessment of its contribution to gastric cancer malignancy.
CCNYL1 encodes a regulatory subunit that activates CDK14 (PFTK1) and CDK16. It assembles with these kinases to phosphorylate the Wnt co-receptor LRP6, enhancing ??-catenin stabilization and transcription of Wnt targets like AXIN2 and MYC. This positions CCNYL1 at the nexus of cell cycle and Wnt/??-catenin signaling. Upstream, CCNYL1 expression is induced by E2F1, MYC, and Wnt3a, while downstream the CCNYL1-CDK14 axis converges on RB1 and E2F targets, modulated by p21/p27. Pathway components include Frizzled, DVL, TCF4, Cyclin D1, and CDK4, linking mitogenic cues to proliferation.
In HGC-27 cells, CCNYL1 knockout disrupts Wnt-driven proliferation by impairing LRP6 phosphorylation and ??-catenin-dependent transcription, potentially reducing cell cycle promoter expression and growth. This model elucidates how CCNYL1 integrates Wnt3a and EGF signals to drive gastric cancer cell proliferation. It also enables evaluation of CDK14-mediated LRP6 phosphorylation dependency and its impact on migration and cell cycle distribution, clarifying CCNYL1’s role in gastric cancer pathogenesis.
These polyclonal knockout cells are suited for Western blotting (CCNYL1, phospho-LRP6, ??-catenin), RT-qPCR (AXIN2, MYC), and TOP/FOP Flash luciferase assays to assess ??-catenin/TCF4 activity. MTT and flow cytometry support proliferation and cell cycle analysis, while Transwell assays examine migration/invasion. Applications include functional dissection of Wnt signaling, CDK inhibitor screening, and target validation. For further details, contact Ascent Research.
