The GOLGA4 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the NCI-H1975 human lung adenocarcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted GOLGA4 gene disruptions, enabling loss-of-function studies of Golgi-mediated trafficking without clonal bias. The polyclonal format preserves the genetic background of the host line and is supplied as a ready-to-use mixed cell population for immediate functional assays.
The parental NCI-H1975 cell line was established from a nonsmoker female lung adenocarcinoma and harbors the EGFR L858R and T790M mutations, representing a clinically relevant model of non-small cell lung cancer with acquired TKI resistance. These cells retain oncogenic EGFR dependency and serve as a robust platform for investigating signaling, proliferation, and drug response in a disease-appropriate context. The line is widely used in NSCLC research and is amenable to a broad range of downstream analyses.
GOLGA4 encodes golgin A4, a Golgi matrix protein that tethers vesicles to the cis-Golgi through interactions with Rab6 and the microtubule motor complex KIF5B?CCLASP1. Its activity is regulated by ARF1 and PKD1, linking upstream signaling to Golgi organization. GOLGA4-mediated tethering is critical for anterograde transport of cargo such as EGFR; its knockout leads to Golgi fragmentation, impaired secretion, and deficient plasma membrane delivery of transmembrane proteins. This disruption broadly affects intracellular transport, cell migration, and growth factor receptor signaling.
In NCI-H1975 cells, GOLGA4 knockout likely diminishes surface EGFR expression, attenuating downstream AKT and ERK activation, and reducing proliferative and migratory capacity. Given that efficient EGFR membrane localization is essential for oncogenic signaling by the L858R/T790M mutant, this model allows interrogation of Golgi-dependent mechanisms influencing TKI sensitivity and acquired resistance. Furthermore, the knockout may alter the secretion of tumor-promoting factors, providing opportunities to study Golgi-driven contributions to the tumor microenvironment and metastatic behavior.
Key applications include western blotting for EGFR and downstream effectors, immunofluorescence to assess Golgi morphology, flow cytometry to measure surface receptor levels, and functional assays such as proliferation, migration, and drug sensitivity testing with EGFR inhibitors. RT-qPCR can be used to monitor transcriptional changes. The polyclonal population supports robust statistical analysis of gene knockout effects. For further information or custom gene-editing services, please contact Ascent Research.
