The CCDC91 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the A-549 human lung adenocarcinoma epithelial cell line, engineered for targeted disruption of the CCDC91 gene. This loss-of-function model enables investigation of CCDC91-dependent processes within a cancer-relevant epithelial context. The polyclonal format preserves genetic heterogeneity inherent to the knockout pool, avoiding clonal selection artifacts, making it suitable for studies that require population-level phenotypic analysis rather than single-clone effects.
A-549 cells are an extensively characterized adherent epithelial cell line derived from a human lung adenocarcinoma. They serve as a standard model in cancer biology, drug discovery, and respiratory epithelial research. These cells express characteristic markers of alveolar epithelial type II pneumocytes and retain key oncogenic mutations. Their epithelial origin and tumorigenic properties make them particularly valuable for investigating the intersection of intracellular trafficking and cancer cell phenotypes, including proliferation, migration, and therapeutic resistance.
CCDC91 functions as an adaptor-binding protein that coordinates with Golgi-localized, ??-ear-containing, Arf-binding (GGA) adaptors, specifically GGA1 and GGA2, at the trans-Golgi network (TGN). Through interactions with clathrin, the AP-1 complex, and the small GTPase ARF1, CCDC91 participates in the selective sorting of cargo proteins, including lysosomal hydrolases, into clathrin-coated vesicles destined for endosomes and lysosomes. This protein acts downstream of ARF1 activation and upstream of endosomal cargo delivery, playing a central role in clathrin-mediated trafficking from the TGN to the endosomal system. Disruption of CCDC91 therefore perturbs this canonical sorting pathway.
In A-549 lung adenocarcinoma cells, CCDC91 knockout is expected to impair Golgi-to-endosome trafficking, potentially leading to mislocalization of lysosomal enzymes, altered receptor recycling, and dysregulation of signaling pathways dependent on endosomal sorting. Such trafficking defects may affect cancer-relevant processes, including cell surface receptor dynamics, extracellular matrix remodeling, and autophagy. The A-549 background provides a disease-specific platform to study how CCDC91 loss influences known cancer hallmarks, such as sustained proliferation and invasion, and may reveal vulnerabilities exploitable for therapeutic intervention in lung adenocarcinoma.
Researchers can employ this polyclonal knockout cell population in a wide range of experimental assays. Co-immunoprecipitation and immunofluorescence microscopy enable investigation of CCDC91??s interactions with GGA1, GGA2, and clathrin, while transferrin uptake assays serve as a functional readout of clathrin-mediated endocytosis. Cell-based assays??including Boyden chamber migration/invasion, proliferation, and drug sensitivity screens??can dissect the role of endosomal trafficking in lung cancer biology. Additionally, transcriptomic profiling via RNA-seq may uncover downstream pathways impacted by CCDC91 loss. For further information or custom orders, please contact Ascent Research.
