The DPCD Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian adenocarcinoma cell line. This product enables loss-of-function studies of the DPCD gene, which encodes cilia and flagella associated protein 45 (CFAP45), a critical factor for ciliary assembly and motility. The polyclonal population carries gene disruption across the cell pool, providing a robust model for investigating DPCD-dependent cellular processes without requiring single-cell clonal isolation. Such polyclonal knockout cells are particularly useful for broad phenotypic screens and functional genomics assays in a heterogeneous cancer cell background.
The MES-OV host cell line is an epithelial ovarian cancer line originally established from a patient with ovarian carcinoma. It displays adherent epithelial morphology and serves as a widely employed model for ovarian cancer biology, including studies on tumorigenesis, metastasis, and therapeutic resistance. MES-OV cells retain key signaling pathways relevant to ovarian pathophysiology, and their ability to form primary cilia makes them a suitable platform for dissecting ciliary functions in the context of malignant transformation. The integration of DPCD knockout in this background allows researchers to specifically interrogate ciliary contributions to ovarian cancer phenotypes.
DPCD/CFAP45 is a core axonemal component essential for the stable assembly of dynein arms and proper ciliary motility. Its transcription is primarily regulated by ciliogenic transcription factors FOXJ1, RFX3, and RFX2. CFAP45 protein interacts directly with intraflagellar transport (IFT) complexes A and B, the chaperone LRRC6, and assembly factor DNAAF1 to facilitate dynein arm preassembly and trafficking into the cilium. Downstream, functional CFAP45 is required for the correct localization and activity of axonemal dynein heavy chains (e.g., DNAH5) and intermediate chains (e.g., DNAI1), as well as proper tubulin incorporation. Disruption of DPCD therefore blocks ciliogenesis and impairs primary cilium-dependent signaling pathways, notably the Hedgehog pathway, with far-reaching consequences for cellular homeostasis.
In the MES-OV ovarian cancer model, loss of DPCD-mediated ciliary functions provides a unique opportunity to dissect the crosstalk between ciliary signaling and oncogenic pathways. Because primary cilia serve as signaling hubs for Hedgehog, Wnt, and other developmental cascades, their absence can alter tumor cell behavior, drug sensitivity, and interactions with the microenvironment. This model thus facilitates the study of ciliopathy-related mechanisms in an epithelial cancer setting, bridging the gap between ciliary biology and ovarian tumor biology. The polyclonal nature of the knockout population preserves some genetic diversity, enabling the identification of dominant phenotypic effects that are reproducible across slightly varied genetic backgrounds.
Typical research applications include functional dissection of ciliary assembly and motility through immunofluorescence detection of ciliary markers (acetylated ??-tubulin, ARL13B), Western blot quantitation of CFAP45 and dynein arm components, and RT-qPCR profiling of ciliogenic transcription factors such as FOXJ1 and target genes like DNAH5. The product is also suited for drug screening campaigns targeting ciliopathy phenotypes, transmission electron microscopy-based ultrastructural analysis of axonemal defects, and co-immunoprecipitation assays to map protein interactions with IFT complexes. Additionally, ciliary motility tracking assays can directly quantify functional defects in the polyclonal population. For more information or to inquire about this product, please contact Ascent Research.
