The GOLM1 Knockout SK-HEP-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population with targeted disruption of the GOLM1 gene in the SK-HEP-1 hepatocellular carcinoma cell line. This loss-of-function model enables investigation of GOLM1??s role in liver cancer biology without clonal selection, preserving population-level heterogeneity for robust functional studies. The ready-to-use format accelerates research on GOLM1-dependent pathways and therapeutic target validation.
SK-HEP-1 cells were established from ascites of a liver adenocarcinoma patient and exhibit endothelial-like properties, making them a relevant model for hepatocellular carcinoma and tumor-endothelial interactions. The cell line retains active EGFR signaling and epithelial-mesenchymal transition (EMT) programs, providing a physiologically appropriate context for examining GOLM1-mediated mechanisms in cancer progression.
GOLM1, a Golgi membrane protein, facilitates EGFR recycling to sustain signaling downstream of ligands such as EGF, HGF, and TGF-??, and transcriptional activation by STAT3. This recycling promotes AKT/mTOR pathway activity, leading to phosphorylation of AKT and mTOR, stabilization of ??-catenin, upregulation of matrix metalloproteinases MMP-2 and MMP-9, and induction of EMT via SNAI1. GOLM1 thus integrates extracellular cues with intracellular machineries driving proliferation, migration, and invasion.
In this SK-HEP-1 background, GOLM1 disruption impairs EGFR trafficking and correspondingly dampens AKT/mTOR signaling. Consequently, the knockout cells exhibit reduced activation of downstream effectors such as ??-catenin and MMPs, leading to diminished proliferative, migratory, and invasive phenotypes. This model therefore allows precise dissection of GOLM1??s contribution to hepatocellular carcinoma aggressiveness and the EMT process.
Researchers can employ this polyclonal knockout population for Western blotting of EGFR, AKT, mTOR, and EMT markers; co-immunoprecipitation of GOLM1?CEGFR complexes; and immunofluorescence to track Golgi and EGFR localization. Functional assays??Transwell migration/invasion, flow cytometric cell cycle and apoptosis analysis, and phospho-signaling profiling??quantify phenotypic outcomes. The cells are also suitable for xenograft tumor growth studies and high-throughput screening of signaling inhibitors. For technical inquiries, please contact Ascent Research.
