The CCDC120 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian endometrioid adenocarcinoma cell line. This product provides a loss-of-function model for the CCDC120 gene, which encodes a coiled-coil domain-containing protein that localizes to centriolar satellites. The polyclonal knockout cells are generated via CRISPR/Cas9-mediated gene disruption, yielding a mixed population that lacks CCDC120 function without single-cell clonal selection. This population-based knockout approach preserves cellular heterogeneity while enabling robust functional studies.
The parental A2780 cell line was originally established from an untreated patient with ovarian endometrioid adenocarcinoma and serves as a well-characterized model for ovarian cancer biology and drug resistance. A2780 cells exhibit epithelial morphology and are widely used to investigate mechanisms of chemoresistance, particularly to platinum-based agents such as cisplatin. They retain key signaling pathways, including Hedgehog, making them suitable for examining ciliary-dependent processes in a cancer context.
CCDC120 functions as a component of the centriolar satellite system, where it interacts with PCM1, CEP290, CEP72, and the kinesin-2 motor complex to organize the trafficking of ciliary proteins. Its activity is induced by RFX transcription factors, Hedgehog ligands, and serum starvation, and it acts upstream of GLI transcription factors and PTCH1, promoting primary cilium assembly and Hedgehog signal transduction. Disruption of CCDC120 impairs ciliogenesis and attenuates signaling downstream of SMO, leading to altered expression of ciliary membrane proteins and Hedgehog target genes. Representative pathway components include IFT88, KIF3A, and GLI1, placing CCDC120 at a critical node linking centriolar satellite dynamics to ciliary signaling.
In the A2780 ovarian cancer background, CCDC120 knockout provides a valuable model to dissect the interplay between centrosomal/ciliary biology and oncogenic signaling. Ovarian cancer cells frequently display aberrant ciliation and Hedgehog pathway activity, both of which have been implicated in tumor progression and drug resistance. By eliminating CCDC120, researchers can assess the dependence of A2780 cells on primary cilium-mediated Hedgehog signaling and explore how loss of ciliary protein trafficking impacts cell migration, invasion, and sensitivity to chemotherapeutics like cisplatin.
These polyclonal knockout cells are suitable for a range of assays, including immunofluorescence staining for ciliary markers such as acetylated tubulin and Arl13b to quantify cilium formation, western blot analysis of Hedgehog effectors like GLI1 and PTCH1, RT?qPCR profiling of ciliary gene expression, and functional assessments of cell migration and invasion. Additionally, drug sensitivity assays with cisplatin can elucidate the contribution of CCDC120 to chemoresistance. For further details or technical inquiries, please contact Ascent Research.
