The CCDC85C Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 gastric carcinoma cell line, in which the CCDC85C gene has been disrupted to create a loss-of-function model. This heterogeneous pool of edited cells avoids clonal selection biases, preserving genetic diversity while ensuring efficient gene silencing. The polyclonal format is well-suited for functional genomics, drug screening, and pathway analysis where representation of multiple editing events is advantageous. The CRISPR/Cas9 system introduces targeted double-strand breaks in CCDC85C, enabling robust and specific gene disruption.
The HGC-27 parental cell line originates from a lymph node metastasis of a gastric adenocarcinoma in a female patient and serves as a classic epithelial model for studying gastric cancer metastasis and tumorigenesis. These cells exhibit characteristics of advanced adenocarcinoma, including dysregulated adhesion and cytoskeletal organization, making them ideal for investigating invasion-associated pathways. HGC-27 is commonly employed to examine Wnt/??-catenin and Rho GTPase signaling, which are central to metastatic progression.
CCDC85C encodes a coiled-coil domain-containing protein that mediates protein-protein interactions and contributes to cellular structural organization. The protein interacts with coiled-coil domain partners and cytoskeletal elements, positioning it as a participant in cytoskeletal remodeling and cell adhesion. Downstream, CCDC85C influences the activity and/or localization of ??-catenin, RhoA, and integrin ??1, molecular factors that coordinate actin dynamics and focal adhesion assembly. Disruption of CCDC85C likely destabilizes these complexes, thereby modulating pathways that control cell migration and invasion. Although its upstream regulation is not fully characterized, CCDC85C may be controlled by cancer-associated transcription factors, and its link to ??-catenin implicates it in Wnt signaling cascades frequently altered in gastric malignancies.
Within the HGC-27 gastric carcinoma context, CCDC85C knockout offers a powerful loss-of-function system to interrogate the contribution of coiled-coil domain-dependent interactions to metastatic cell behavior. The integrated analysis of ??-catenin, RhoA, and integrin ??1 in these knockout cells can reveal how CCDC85C couples cytoskeletal architecture to adhesion-dependent signaling and gene expression. This model thus enables dissection of the mechanistic underpinnings of cell adhesion, cytoskeletal reorganization, and motility during gastric adenocarcinoma progression, with potential implications for identifying novel molecular vulnerabilities.
Research applications for this product encompass functional genomics of gastric cancer, protein-protein interaction studies, metastasis research, and drug target discovery. Users can perform western blotting to monitor ??-catenin and RhoA pathway markers, cell migration and adhesion assays to evaluate phenotypic changes, immunofluorescence to visualize cytoskeletal disruption, and co-immunoprecipitation to map CCDC85C interaction networks. The polyclonal population provides a realistic heterogeneous background for screening therapeutic agents and genetic modifiers. For further information or custom project support, please contact Ascent Research.
