The CCDC127 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human CCDC127 gene in the A2780 ovarian carcinoma epithelial cell line. This product provides a heterogeneous pool of cells with gene disruption, enabling loss-of-function studies without single-cell cloning artifacts. The polyclonal format preserves population-level diversity while abrogating CCDC127 protein expression, and it is suitable for experiments where clonal variability is less critical than robust gene silencing. The cells are generated using a validated CRISPR/Cas9 methodology that introduces targeted gene disruption, resulting in a stable knockout model for investigating primary cilia biology and related signaling pathways.
The host A2780 cell line is a well-established human ovarian carcinoma model derived from an untreated patient. These adherent epithelial cells are widely utilized in ovarian cancer research, including studies of tumor cell signaling, drug resistance, and tumor microenvironment interactions. A2780 cells retain characteristics of high-grade serous ovarian carcinoma and offer a relevant cellular context for evaluating gene function in ovarian cancer pathogenesis. Their genetic background, combined with the CRISPR-mediated CCDC127 knockout, enables dissection of molecular mechanisms at the intersection of ciliogenesis and oncogenic signaling.
CCDC127 encodes a protein that localizes to the basal body and centrosome, functioning as an essential component of primary cilium assembly and maintenance. The protein interacts directly with the BBSome complex and intraflagellar transport (IFT) proteins, which are critical for ciliary trafficking and signaling. Upstream regulators include the RFX family of transcription factors and FOXJ1, both master regulators of ciliogenic gene expression. Downstream, CCDC127 loss disrupts ciliary membrane composition and attenuates Hedgehog pathway activation, evidenced by reduced GLI transcription factor processing and target gene transcription. This disruption also impacts Wnt signaling effectors, linking CCDC127 to a broad network of ciliary signaling cascades.
In the ovarian cancer context, primary cilia have been shown to modulate proliferation, migration, and drug sensitivity, though their roles are cell-type and context dependent. The CCDC127 knockout in A2780 cells provides a model to study how ciliary dysfunction influences ovarian carcinoma phenotypes. Because A2780 cells normally form primary cilia under serum-starvation conditions, the knockout enables investigation of cilia-dependent versus cilia-independent effects on oncogenic pathways. This model can be used to test whether cilia loss alters response to chemotherapeutics or targeted agents, and to explore the crosstalk between ciliary signaling and ovarian cancer driver mutations.
This polyclonal knockout product is suited for a range of biomedical research applications. Primary uses include the study of ciliopathy mechanisms??especially Joubert syndrome??cancer cilia biology, and Hedgehog/Wnt pathway modulation. Representative assays include western blotting to verify CCDC127 depletion, immunofluorescence microscopy for cilia markers such as Arl13b and acetylated tubulin, RT-qPCR profiling of ciliary gene expression, and functional ciliogenesis assays. Additional applications encompass cell proliferation and apoptosis assays to assess phenotypic outcomes, and high-content screening for cilia-modulatory compounds. For further technical details or ordering information, please contact Ascent Research.
