CCDC82 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-mediated polyclonal knockout cell population targeting the CCDC82 gene in the HGC-27 human gastric carcinoma cell line. This loss-of-function model is designed to facilitate functional interrogation of CCDC82, a gene encoding a coiled-coil domain-containing protein implicated in cytoskeletal dynamics and cell motility. The polyclonal format yields a heterogeneous pool of gene-edited cells, enabling robust pooled analysis of gene disruption effects without clonal selection bias.
The HGC-27 cell line is a poorly differentiated, metastatic gastric adenocarcinoma model originally isolated from a lymph node metastasis. It maintains wild-type TP53 and is extensively employed in gastric cancer research for studying proliferation, migration, and invasion. The metastatic origin of HGC-27 makes it particularly suitable for investigating genes involved in tumor dissemination and the epithelial-to-mesenchymal transition.
CCDC82 is characterized by coiled-coil domains that mediate protein?Cprotein interactions essential for cytoskeletal organization and signal transduction. It functions downstream of growth factor receptors such as EGFR and is regulated by transcription factors including MYC, linking it to MAPK pathway activity. CCDC82 interacts with cytoskeletal proteins (e.g., myosin, dynein) and cell adhesion molecules, converging on key effectors such as RhoA, ROCK, FAK, SRC, paxillin, and actin. Through these interactions, CCDC82 modulates actin polymerization and focal adhesion dynamics, thereby influencing cell migration and invasion. Its role in Rho GTPase signaling positions it as a critical node in the coordination of cytoskeletal remodeling and cell adhesion.
In the context of HGC-27 gastric cancer cells, disruption of CCDC82 is predicted to impair actin reorganization and attenuate migratory and invasive capacity, consistent with its proposed function in metastatic progression. This polyclonal knockout model provides a physiologically relevant system to dissect CCDC82-dependent signaling mechanisms underlying gastric cancer aggressiveness. The availability of this model enables systematic investigation of how loss of CCDC82 affects the RhoA/ROCK and FAK/SRC pathways, which are central to cytoskeletal control and cell motility.
Researchers can utilize this knockout product in a range of functional assays, including wound healing, Transwell migration, and Matrigel invasion studies, to quantify motility defects. Protein interaction networks can be probed via co-immunoprecipitation, while immunofluorescence microscopy for F-actin allows visualization of actin cytoskeleton architecture. Transcriptomic analysis through RNA-seq, complemented by RT-qPCR and Western blotting, supports expression profiling and target validation. These polyclonal CCDC82 knockout cells are a valuable tool for therapeutic target validation and mechanistic studies in gastric cancer and metastatic carcinoma. For further details, please contact Ascent Research.
