The CCDC91 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-mediated gene disruption pool targeting the coiled-coil domain-containing protein 91 (CCDC91) locus in the human A2780 ovarian carcinoma cell line. This polyclonal knockout cell population provides a heterogeneous collection of edited cells, each carrying diverse loss-of-function mutations, offering a physiologically relevant model to study gene function without the clonal bias of single-cell-derived lines. Researchers can leverage this product to interrogate the cellular consequences of CCDC91 ablation in a well-established ovarian cancer background.
The A2780 cell line, originally derived from an untreated patient with ovarian endometrioid adenocarcinoma, serves as a widely adopted model for epithelial ovarian cancer biology. Its retention of key oncogenic signaling cascades and intact membrane trafficking machinery makes it particularly suitable for dissecting intracellular transport pathways. As a human epithelial cell system, A2780 recapitulates the pathological context of ovarian carcinoma, enabling the assessment of gene disruptions on tumor cell behavior and protein homeostasis.
CCDC91 encodes an adaptor protein that orchestrates vesicle trafficking from the trans-Golgi network (TGN) to endosomes by bridging Golgi-localized, ??-ear-containing, ADP-ribosylation factor-binding proteins (GGA1 and GGA2) with the clathrin coat and the AP-1 complex. This molecular linkage facilitates cargo sorting and vesicle formation, directing specific transmembrane proteins, such as epidermal growth factor receptor (EGFR) and transferrin receptor, toward endosomal compartments. Consequently, CCDC91 knockout likely disrupts these interactions, leading to impaired clathrin recruitment, defective vesicle budding, and altered subcellular distribution of cargo receptors.
In the A2780 ovarian cancer milieu, dysregulated membrane protein trafficking contributes to malignant phenotypes, including enhanced receptor signaling, cell migration, and invasion. Disabling CCDC91 function may perturb the surface levels and recycling of pro-oncogenic receptors, thereby attenuating downstream proliferative and metastatic cascades. The polyclonal knockout pool mirrors the genetic heterogeneity present in therapeutic gene targeting, providing a robust system to evaluate the collective impact of CCDC91 loss on cancer cell pathobiology and to identify compensatory mechanisms that may arise upon trafficking network perturbation.
This knockout cell product supports a broad spectrum of experimental applications, including immunofluorescence microscopy to visualize Golgi and endosomal marker redistribution, co-immunoprecipitation to assess residual CCDC91?CGGA protein interactions, flow cytometry for quantifying surface receptor abundance, and functional assays such as wound-healing migration and Matrigel invasion. Additionally, RNA sequencing can reveal transcriptomic adaptations following CCDC91 disruption. For technical specifications, lot-specific quality control data, or customized support, please contact Ascent Research.
