The GOLPH3L Knockout A-549 Polyclonal Cells comprise a population of A-549 lung adenocarcinoma cells subjected to CRISPR/Cas9-mediated disruption of the endogenous GOLPH3L gene. As a polyclonal knockout pool, this product circumvents clonal selection biases, offering a heterogeneous model that reflects editing outcome diversity. It is intended for functional studies requiring robust, population-based readouts of GOLPH3L-dependent mechanisms.
The A-549 cell line is a human lung adenocarcinoma epithelial model derived from a 58-year-old Caucasian male. Widely used in oncology and pharmacology, A-549 cells serve as a standard host for studying tumor biology, drug metabolism, and respiratory cell physiology. Their adherent growth and compatibility with molecular techniques make them an ideal background for creating CRISPR-edited knockout populations to interrogate genes implicated in lung cancer progression.
GOLPH3L is a trans-Golgi network?Cassociated phosphoprotein that participates in Golgi-to-plasma membrane trafficking. It interacts with the retromer subunit Vps35, its paralog GOLPH3, and phosphoinositide PI4P to coordinate vesicle budding. Signaling input from growth factors through PI3K-Akt is believed to regulate GOLPH3L function. Downstream, GOLPH3L modulates mTORC1 kinase activity, influencing the phosphorylation of S6K and 4E-BP1, and thereby coupling Golgi trafficking to cell growth and proliferation. Additionally, GOLPH3L impacts protein glycosylation and sphingolipid biosynthesis, processes critical for membrane receptor presentation and signaling.
In the context of A-549 adenocarcinoma cells, GOLPH3L knockout enables dissection of its putative tumor-modulatory roles. The disruption is expected to alter mTORC1 signaling and Golgi-dependent glycosylation, both commonly altered in lung cancer. These polyclonal cells provide a physiologically relevant system to study how GOLPH3L loss affects proliferation, survival, and therapeutic response, while the polyclonal nature better represents the heterogeneity observed in tumors.
Typical applications include Western blot analysis of mTOR pathway activation (e.g., phospho-S6K, phospho-4E-BP1), immunofluorescence imaging of Golgi morphology, and flow cytometry for cell cycle and apoptosis. Migration and invasion assays can assess metastatic behavior, while glycosylation profiling characterizes post-translational modifications. Drug sensitivity studies with cisplatin or EGFR inhibitors evaluate resistance mechanisms. By integrating Golgi biology with mTOR signaling, this model is valuable for studying tumor-suppressive functions, adaptive signaling, and synthetic lethality screens. For additional details or custom queries, please contact Ascent Research.
