The GOLPH3 Knockout A-549 Polyclonal Cells provide a CRISPR/Cas9-mediated gene-disrupted pool of human lung adenocarcinoma A-549 cells. As a polyclonal population, this model avoids single-clone biases and preserves heterogeneous editing outcomes, enabling robust loss-of-function studies of GOLPH3.
The parental A-549 cell line is a KRAS G12S-mutant human lung adenocarcinoma epithelial model widely used in cancer biology. Its adherent growth and epithelial origin make it suitable for investigating oncogenic signaling pathways, including those intersecting with Golgi-resident proteins.
GOLPH3 is an oncogenic phosphoprotein that binds PI4P and MYO18A at the trans-Golgi, tethering membranes to the actin cytoskeleton to drive vesicle budding and trafficking. It also interacts with coatomer and regulates glycosyltransferase localization, impacting protein glycosylation. Overexpression hyperactivates PI3K/AKT/mTOR signaling, enhancing phosphorylation of mTORC1, S6K, and 4E-BP1, thereby promoting proliferation and survival. Furthermore, GOLPH3 influences the DNA damage response and mitotic Golgi disassembly, processes subverted in cancer.
In KRAS-driven lung adenocarcinoma, elevated GOLPH3 fosters tumor progression and chemoresistance. Disrupting GOLPH3 in A-549 cells allows dissection of Golgi-dependent contributions to DNA damage response, mitotic Golgi disassembly, and sensitivity to cisplatin or EGFR inhibitors, addressing key therapeutic resistance mechanisms.
This knockout pool supports diverse assays: immunoblotting and RT-qPCR for knockout validation, immunofluorescence (GM130, TGN46) for Golgi morphology, colony formation and transwell assays for tumorigenicity, and flow cytometry for cell cycle/apoptosis. Phospho-signaling analysis (p-AKT, p-S6K) and drug-sensitivity profiling with cisplatin or EGFR inhibitors directly link GOLPH3 to oncogenic output. These applications enable functional characterization and target validation in lung adenocarcinoma. For further inquiries, contact Ascent Research.
