The GOLM1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 near-haploid human chronic myeloid leukemia cell line. This product features targeted disruption of the GOLM1 (Golgi membrane protein 1, also known as GP73) gene, providing a loss-of-function model for investigating the cellular roles of this Golgi-resident protein. The polyclonal format captures diverse editing outcomes, enabling robust population-level studies.
HAP1 cells were originally isolated from the KBM-7 chronic myeloid leukemia line and adapted for adherent monolayer culture. Their near-haploid karyotype, with only one copy of most chromosomes, facilitates efficient knockout generation because disruption of a single allele is sufficient to abrogate gene function. This characteristic, combined with their well-characterized signaling networks and high-throughput screening compatibility, makes HAP1 an exceptional host for functional genomic studies. The cells retain core cancer-relevant pathways, widely used in oncogenic signaling research and drug discovery.
GOLM1 encodes a type II transmembrane protein predominantly localized to the cis-Golgi, where it plays essential roles in vesicular trafficking, Golgi stack maintenance, and secretory pathway regulation. Mechanistically, GOLM1 interacts with components of the COPI vesicle coat and ARF GTPases, facilitating retrograde transport and cargo sorting. In hepatocellular carcinoma, GOLM1 expression is induced by hepatitis B and C virus proteins, interleukin-6 (IL-6), and growth factors through activation of STAT3 and NF-kB transcription factors. Once upregulated, GOLM1 feeds forward to reinforce STAT3 and NF-kB signaling, leading to increased transcription of cyclins and matrix metalloproteinases (MMPs), which promote cell cycle progression, migration, and invasion. Furthermore, GOLM1 is secreted and detected as a serum biomarker, reflecting Golgi function and tumor burden.
In the HAP1 background, GOLM1 knockout eliminates endogenous protein expression, providing a defined system to dissect its roles in Golgi architecture and oncogenic signaling without interference from liver-specific factors. Despite their hematopoietic origin, HAP1 cells maintain a fully functional Golgi apparatus and secretory machinery, enabling detailed analysis of GOLM1-dependent trafficking events. This model allows researchers to examine how loss of GOLM1 alters Golgi morphology and downregulates STAT3/NF-kB pathway activity, providing insights into its oncogenic mechanisms.
This knockout population is suited for a broad range of investigations, including liver cancer biomarker discovery, cancer cell signaling dissection, and Golgi trafficking analysis. Key experimental applications include western blotting and RT-qPCR for confirming target disruption and measuring downstream effectors, cell proliferation and migration/invasion assays to assess functional consequences, and STAT3/NF-kB dual-luciferase reporter assays to quantify pathway activation. Immunofluorescence microscopy allows visualization of Golgi morphological changes, while antibody-based detection methods support biomarker quantification. The polyclonal format is advantageous for pooled screening approaches. For further information or technical support, please contact Ascent Research.
