The CCDC14 Knockout HGC-27 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene disruption targeting CCDC14, yielding a heterogeneous pool of edited cells suitable for functional studies. The polyclonal format avoids clonal selection artifacts and maintains population-level representation of knockout phenotypes, making it ideal for initial screening of cilia-related signaling pathways and drug response assays.
HGC-27 is a widely employed epithelial carcinoma model originally isolated from a lymph node metastasis of a human gastric adenocarcinoma. This cell line retains key characteristics of gastric cancer, including deregulated proliferation, altered migration, and resistance to apoptosis. As a metastatic derivative, HGC-27 provides a relevant background for exploring tumor progression mechanisms and the role of primary cilia in aggressive gastric cancer phenotypes. Its well-documented culture requirements and genomic profile support reproducible experimental conditions across independent studies.
CCDC14 encodes a centrosomal protein that localizes to the distal appendages of the mother centriole and is essential for primary cilium assembly. CCDC14 interacts with distal appendage proteins such as CEP83, CEP89, and SCLT1, and facilitates recruitment of the IFT-B complex and BBSome during ciliogenesis. Loss of CCDC14 function abrogates primary cilium formation, thereby attenuating Hedgehog signaling. In the canonical Hedgehog pathway, ligand SHH binds to PTCH1, relieving suppression of SMO. SMO activation leads to nuclear translocation of GLI transcription factors, including GLI1, which promote expression of target genes such as CCND1 and BCL2. CCDC14 operates upstream of this cascade, and its disruption impairs GLI-mediated transcription, providing a direct link between centrosome biology and signal transduction.
In the HGC-27 gastric cancer context, CCDC14 knockout disrupts primary cilium-dependent Hedgehog signaling, which may influence tumor cell proliferation, survival, and migration. Gastric cancer cells often exhibit aberrant Hedgehog pathway activity, and ciliopathy-related mechanisms are emerging as modulators of oncogenic signaling. By abolishing ciliogenesis, this polyclonal knockout model enables dissection of cilium-specific contributions to HGC-27 pathobiology, independent of other centrosomal functions. It serves as a powerful tool for evaluating the dependency of gastric cancer cells on cilia-driven pathways and for testing inhibitors that target upstream or downstream nodes of the Hedgehog axis.
This polyclonal CCDC14 knockout cell population is suited for a range of research applications, including investigation of cilia-dependent signaling in gastric cancer, Hedgehog pathway inhibition studies, and centrosome biology. Representative assays include immunofluorescence staining for primary cilia markers, qPCR analysis of GLI target genes (e.g., CCND1, BCL2), western blotting for SHH pathway components, cell viability assays, and migration assays. The model supports both genetic and pharmacological rescue experiments, as well as combinatorial drug screens. For additional technical information or to discuss custom cell engineering projects, please contact Ascent Research.
