The GOLM1 Knockout A?549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human A-549 lung adenocarcinoma cells with targeted disruption of the GOLM1 gene. This heterogeneous pool of edited cells collectively abrogates GOLM1 function, providing a loss-of-function model suitable for population-based studies without single-cell clonal selection.
The parental A?549 cell line, derived from a human lung adenocarcinoma, harbors a KRAS G12S mutation and a hypotriploid karyotype. These epithelial cells are a widely used in vitro model for non-small cell lung cancer (NSCLC), particularly for investigating KRAS-driven oncogenic signaling, drug response, and metastasis.
GOLM1 is a Golgi-resident membrane protein involved in protein trafficking and glycosylation. It interacts with EGFR to enhance receptor recycling, thereby sustaining downstream AKT and ERK1/2 signaling, which drives proliferation, EMT, and metastasis. GOLM1 expression is regulated by STAT3 in response to IL-6 or viral proteins (HBV, HCV). Downstream, it promotes activation of AKT, ERK1/2, and matrix metalloproteinases (MMPs). It also associates with actin-binding and Golgi matrix proteins to coordinate vesicular transport and cytoskeletal dynamics.
In A?549 cells, which possess constitutive KRAS signaling, GOLM1 disruption attenuates EGFR recycling and reduces phospho-AKT and phospho-ERK levels, leading to diminished cell proliferation and migration/invasion. This polyclonal knockout model thus provides a relevant system to dissect GOLM1-dependent oncogenic mechanisms and the interplay between Golgi-mediated trafficking and mitogenic signaling in NSCLC.
Applications include western blotting and RT-qPCR for confirmation of gene disruption and pathway analysis; cell proliferation and Transwell assays to quantify growth and motility defects; phospho-AKT/ERK profiling; and EGFR recycling assays. This cell population is also suitable for high-throughput drug screening targeting the GOLM1-EGFR axis. For technical inquiries, contact Ascent Research.
