The CCDC120 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line. This product provides a loss-of-function model for the CCDC120 gene, generated through CRISPR/Cas9-mediated gene disruption of the endogenous CCDC120 locus. The polyclonal knockout population is supplied as a pool of edited cells, offering a genetically heterogeneous knockout background suitable for functional studies where monoclonal isolation is not required. The knockout model enables investigation of CCDC120-dependent cellular processes in an epithelial cancer context.
The HGC-27 host cell line originates from a poorly differentiated gastric adenocarcinoma metastatic to lymph node, exhibiting an epithelial morphology and tumorigenic properties in vivo. This cell line serves as a well-characterized model for gastric adenocarcinoma, particularly in the study of invasion, metastasis, and epithelial malignancy. Its origin from a metastatic site renders it especially valuable for dissecting molecular mechanisms underlying tumor dissemination and aggressive behavior.
CCDC120 encodes a coiled-coil domain-containing protein that localizes to the centrosome and basal body, where it plays a critical role in primary cilium biogenesis and ciliary protein trafficking. Mechanistically, CCDC120 interacts with CEP290 and RPGR, forming complexes that facilitate ciliogenesis and modulate Hedgehog signaling. Upstream, CCDC120 expression is predicted to be regulated by RFX family transcription factors. Downstream, functional CCDC120 promotes efficient ciliary trafficking of signaling components such as SMO and GLI transcription factors, thereby influencing GLI-mediated transcriptional outputs. Disruption of CCDC120 impairs primary cilium formation and reduces Hedgehog pathway responsiveness, connecting this gene to broader ciliopathy mechanisms.
In the gastric adenocarcinoma background, CCDC120 knockout provides a unique tool to dissect how primary cilia influence tumor cell behavior. Emerging evidence suggests that ciliary signaling can affect proliferation, migration, and invasion in cancer cells. By ablating CCDC120 in HGC-27 cells, researchers can examine cilia-dependent modulation of the Hedgehog pathway in a metastatic epithelial context. This model may reveal CCDC120 contributions to tumorigenic properties and help clarify the role of aberrant ciliogenesis in gastric cancer progression.
Applications include investigation of ciliary signaling roles in gastric cancer, functional studies of CCDC120 in tumorigenesis and metastasis, ciliopathy disease modeling, and screening for cilia-dependent drug sensitivities. Representative assays include immunofluorescence for cilia visualization, Western blotting for CCDC120 detection, migration and invasion assays, RNA-seq for transcriptomic profiling, flow cytometry, and Hedgehog pathway inhibitor sensitivity testing. For further information or to request a quotation, please contact Ascent Research.
