This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A2780 ovarian carcinoma cell line, featuring targeted disruption of the CCDC97 gene. The polyclonal format provides a heterogeneous loss-of-function model in which gene editing has been applied across a bulk population, preserving biological variability while eliminating CCDC97 protein expression. As a validated knockout tool, this population enables robust functional studies without clonal selection artifacts, making it suitable for experiments requiring a representative distribution of edited alleles in an ovarian cancer background.
The A2780 cell line was established from an untreated patient with ovarian carcinoma and is widely utilized as a model of ovarian surface epithelial-derived malignancy. These cells retain key characteristics of high-grade serous ovarian carcinoma, including epithelial morphology, sensitivity to platinum-based chemotherapeutics, and relevant oncogenic signaling pathways. The ovarian surface epithelium gives rise to the majority of ovarian cancers, and A2780 cells serve as a standard platform for investigating tumor cell biology, drug response, and metastatic mechanisms.
CCDC97 encodes a coiled-coil domain-containing protein that localizes to the ciliary axoneme, where it is essential for cilia assembly and motility. CCDC97 functions within a network regulated by transcription factors such as FOXJ1, RFX3, and RFX2, which drive ciliogenic gene expression. Downstream, CCDC97 supports Hedgehog signaling by enabling proper trafficking of pathway components like SMO and the GLI transcription factors; loss of CCDC97 impairs GLI1 and GLI2 activation. Additionally, CCDC97 influences Wnt/??-catenin signaling, as ciliary defects can alter ??-catenin stability and AXIN2 expression. The protein interacts with axonemal dynein components, radial spoke proteins, and intraflagellar transport complex B proteins including IFT88 and IFT140, while also intersecting with ciliopathy-associated factors such as BBS4.
In the context of ovarian carcinoma, cilia-dependent signaling pathways have been implicated in tumor progression, chemoresistance, and cell migration. By disrupting CCDC97 in A2780 cells, researchers can model ciliary dysfunction within an ovarian cancer environment, revealing how loss of primary cilia affects Hedgehog and Wnt signal transduction. This knockout population allows dissection of ciliopathy-like phenotypes in cancer, such as altered proliferation rates, migratory capacity, and sensitivity to cisplatin. The model thus bridges cilia biology and ovarian cancer research, offering a unique tool to explore whether ciliary defects contribute to malignancy-associated signaling perturbations.
These CCDC97 knockout polyclonal cells support a wide range of experimental applications, including mechanistic studies of cilia-dependent Hedgehog and Wnt signaling cascades, functional analysis of ciliopathy genes in cancer, and drug sensitivity profiling using cisplatin. Common readouts include GLI-dependent luciferase assays, ??-catenin/TCF reporter assays, cell proliferation via MTT, transwell migration assays, and immunofluorescence staining for ciliary markers such as acetylated ??-tubulin and ARL13B. Protein-level validation is performed by western blotting for CCDC97. Researchers employing these cells can investigate how ciliary axonemal components modulate oncogenic pathways and therapeutic responses. For additional information or technical support, please contact Ascent Research.
