This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, engineered for targeted disruption of the CCDC71L gene. The polyclonal format provides a genetically heterogeneous pool of knockout cells, enabling robust functional studies without the clonal selection biases associated with single-cell-derived lines. This loss-of-function model is designed for researchers investigating the biological role of CCDC71L in gastric cancer, a gene for which functional annotation remains limited.
The HGC-27 cell line was originally established from lymph node metastasis of a patient with gastric adenocarcinoma and is widely employed as a model system for studying metastatic gastric cancer biology, including cell proliferation, invasion, and therapeutic resistance mechanisms. Its use in drug response assays and signaling studies makes it a relevant background for examining the impact of CCDC71L disruption on tumor cell behavior in a clinically pertinent context.
CCDC71L encodes a coiled-coil domain-containing protein of unknown function, with in silico predictions suggesting a role in mediating protein-protein interactions, possibly contributing to cytoskeletal dynamics or ciliary architecture. Although its upstream regulators and downstream targets remain undefined in gastric cancer, loss-of-function studies in HGC-27 cells may illuminate its participation in signaling networks that control tumor-relevant phenotypes, potentially intersecting with pathways involved in cell adhesion and motility.
By disrupting CCDC71L in the metastatic HGC-27 background, researchers can interrogate how this putative scaffolding protein influences key malignant properties such as anchorage-independent growth, migration, and invasion. Given the limited characterization of CCDC71L, this polyclonal knockout model serves as a critical tool for hypothesis generation and validation, particularly for uncovering novel molecular vulnerabilities in gastric adenocarcinoma and for identifying synthetic lethal interactions with existing chemotherapies.
Typical applications include Western blotting and RT-qPCR to confirm gene disruption and assess transcriptional consequences, cell proliferation and migration/invasion assays to evaluate phenotypic impacts, and drug sensitivity profiling to explore chemotherapeutic responses. Additionally, RNA-seq-based transcriptome profiling can reveal downstream gene expression changes, facilitating the discovery of CCDC71L-associated networks. For technical inquiries or custom requests, please contact Ascent Research.
