The GOLM1 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the GOLM1 gene in the human NCI-H1975 lung adenocarcinoma cell line. This loss-of-function model provides a means to dissect GOLM1-dependent cellular mechanisms, making it suitable for advanced cancer cell signaling and secretion studies.
NCI-H1975 is an epithelial cell line isolated from non-small cell lung cancer and carries an activating EGFR L858R mutation, rendering cells responsive to EGFR tyrosine kinase inhibitors. Frequently used as a model for lung adenocarcinoma, it retains EGFR-driven oncogenic signaling, enabling investigation of targeted therapy responses and resistance mechanisms.
GOLM1 encodes a Golgi membrane protein critical for Golgi structure maintenance, protein trafficking, and cell adhesion. It is activated by EGF, TGF-??, HGF, STAT3, c-Myc, and HIF1??, and interacts with Golgi matrix components including GOLGA2 (GM130), p115, and Rab proteins. GOLM1 promotes cancer invasion and metastasis by upregulating MMP2 and MMP9 secretion and by modulating Rho GTPases to remodel the actin cytoskeleton. Downstream, it enhances PI3K/AKT and MAPK/ERK signaling downstream of EGFR, while repressing E-cadherin and inducing vimentin, facilitating epithelial-mesenchymal transition.
In NCI-H1975 cells, GOLM1 knockout likely disrupts Golgi integrity and secretory trafficking, reducing MMP-dependent ECM degradation and attenuating AKT and ERK activation. This impairs cell migration, invasion, and EMT, and may sensitize cells to EGFR inhibitors. The knockout thus serves as a relevant model to examine crosstalk between Golgi-mediated secretion and oncogenic kinase signaling in lung adenocarcinoma.
This polyclonal knockout population supports applications in Golgi biology, protein secretion, migration/invasion mechanisms, drug resistance, and biomarker discovery. Compatible with Western blotting, RT-qPCR, immunofluorescence, flow cytometry, wound healing, Transwell invasion, co-immunoprecipitation, phospho-signaling analysis, and EGFR inhibitor viability assays, these cells offer a versatile platform for mechanistic studies. For additional information, contact Ascent Research.
