This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GOPC gene in the human A-549 lung adenocarcinoma cell line. The polyclonal knockout cells provide a heterogeneous loss-of-function model for studying GOPC-dependent cellular processes without requiring single-cell cloning or selection of a discrete clone.
The A-549 host cell line is derived from a human lung adenocarcinoma and exhibits adherent epithelial morphology, a KRAS-activating mutation, and wild-type p53 status. These cells are widely employed as a model for non-small cell lung cancer (NSCLC) and respiratory epithelial biology, offering a relevant genetic context for examining oncogenic signaling, tumor cell migration, and drug resistance mechanisms.
GOPC encodes a scaffold protein that orchestrates Golgi organization and intracellular trafficking through association with the retromer complex component VPS35 and the autophagy machinery, including ATG16L1 and ULK1. GOPC functions downstream of EGFR activation and PDGF signaling to modulate endocytic recycling of transmembrane receptors, while also regulating mTORC1/AMPK signaling and autophagy flux. Disruption of GOPC consequently alters EGFR degradation kinetics, retromer-dependent trafficking, and autophagy initiation, thereby influencing cell polarity and migration.
In the KRAS-mutant A-549 background, GOPC knockout serves as a valuable model for interrogating how Golgi fragmentation and aberrant endosomal recycling contribute to NSCLC progression. Loss of GOPC is predicted to impair EGFR recycling and mTOR-mediated growth signaling, which may affect proliferation and invasive capacity. Moreover, this model allows investigation of autophagy regulation in the context of oncogenic KRAS, and the potential role of GOPC in therapeutic resistance and Golgi fragmentation-associated pathologies, including schizophrenia.
This polyclonal knockout cell product is suitable for intracellular trafficking studies using immunofluorescence-based analysis of Golgi morphology and EGFR colocalization, as well as autophagy flux assays such as LC3 turnover measurements. Researchers can employ western blotting to monitor GOPC, VPS35, mTOR pathway components, and autophagy markers, and functional assays to assess cell migration, invasion, and proliferation. The model supports drug resistance studies and exploration of upstream regulators including PDGF and EGFR. For further information, please contact Ascent Research.
